首页 > 最新文献

Acta histochemica最新文献

英文 中文
Corrigendum to "MicroRNA-146b-5p suppresses cholangiocarcinoma cells by targeting TRAF6 and modulating p53 translocation" [Acta Histochem. (2021) 123 7 151793]. MicroRNA-146b-5p 通过靶向 TRAF6 和调节 p53 转位抑制胆管癌细胞》[Acta Histochem. (2021) 123 7 151793]的更正。
IF 2.3 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-11-09 DOI: 10.1016/j.acthis.2024.152214
Yiyue Ren, Xiaoyan Wang, Tong Ji, Xiujun Cai
{"title":"Corrigendum to \"MicroRNA-146b-5p suppresses cholangiocarcinoma cells by targeting TRAF6 and modulating p53 translocation\" [Acta Histochem. (2021) 123 7 151793].","authors":"Yiyue Ren, Xiaoyan Wang, Tong Ji, Xiujun Cai","doi":"10.1016/j.acthis.2024.152214","DOIUrl":"https://doi.org/10.1016/j.acthis.2024.152214","url":null,"abstract":"","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":" ","pages":"152214"},"PeriodicalIF":2.3,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142611924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Histological and cytochemical analysis of the brain under conditions of hypobaric hypoxia-induced oxygen deficiency in albino rats 白化大鼠低压缺氧缺氧条件下脑的组织学和细胞化学分析
IF 2.5 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2023-11-17 DOI: 10.1016/j.acthis.2023.152114
Ruzanna Shushanyan, Anna Grigoryan, Tamara Abgaryan, Anna Karapetyan

High altitude sickness is a life-threatening disease that occurs among acclimatized individuals working or living at a high altitude accompanied by hypobaric hypoxia exposure. The prolonged influence of hypobaric hypoxia on the brain may trigger neuronal damage and cell death due to an oxygen deficiency. The purpose of the current study was to investigate the histomorphological changes in the hippocampus, cerebral cortex, cerebellar cortex, and striatum of the rat’s brain following chronic hypobaric hypoxia. Fourteen albino rats were used for this investigation. The animals were exposed to chronic hypobaric hypoxia in the special decompression chamber at an altitude of 7000 m for 7 days. The histological analysis was conducted via toluidine staining and silver impregnation. DNA damage and cell apoptosis were assessed via Feulgen staining. The histochemical assessment revealed increased dark neurons in the hippocampus with cell swelling. Silver impregnation showed increased argyrophilic neurons in the cerebellar cortex, striatum, CA1 subfield of the hippocampus, and cerebral cortex. The cytochemical analysis determined the increased apoptotic cells with hyperchromatic condensation and pyknosis in the hippocampus subfields and cerebral cortex. In addition, it has been observed that hypoxia has resulted in small hemorrhages and perivascular edema within the cerebellar and cerebral cortex.

The results indicate brain injury observed in the various parts of the brain towards hypobaric hypoxia, however, the hippocampus showed greater vulnerability against hypoxic exposure in comparison to the striatum, cerebellum, and cerebral cortex. These changes support our insights regarding brain intolerance under conditions of hypoxia-induced oxygen deficiency and its histomorphological manifestations.

高原病是一种危及生命的疾病,发生在适应高海拔工作或生活的个体中,伴随着低气压缺氧暴露。长期的低气压缺氧对大脑的影响可能会引起神经元损伤和因缺氧而导致的细胞死亡。本研究旨在探讨慢性低压缺氧后大鼠脑海马、大脑皮层、小脑皮层和纹状体的组织形态学变化。本研究采用14只白化大鼠。在海拔7000米的专用减压舱内进行慢性低压缺氧治疗7天。采用甲苯胺染色和银浸渍法进行组织学分析。Feulgen染色观察DNA损伤及细胞凋亡情况。组织化学评价显示海马暗神经元增多,细胞肿胀。银浸渍显示小脑皮层、纹状体、海马CA1亚区和大脑皮层的嗜银神经元增加。细胞化学分析表明,海马亚区和大脑皮层凋亡细胞增多,并伴有高染色凝集和固缩。此外,已经观察到缺氧导致小脑和大脑皮层的小出血和血管周围水肿。结果表明,在低压缺氧下,大脑的各个部位都出现了脑损伤,然而,与纹状体、小脑和大脑皮层相比,海马体对缺氧暴露表现出更大的脆弱性。这些变化支持了我们关于缺氧诱导的缺氧条件下脑不耐受及其组织形态学表现的见解。
{"title":"Histological and cytochemical analysis of the brain under conditions of hypobaric hypoxia-induced oxygen deficiency in albino rats","authors":"Ruzanna Shushanyan,&nbsp;Anna Grigoryan,&nbsp;Tamara Abgaryan,&nbsp;Anna Karapetyan","doi":"10.1016/j.acthis.2023.152114","DOIUrl":"https://doi.org/10.1016/j.acthis.2023.152114","url":null,"abstract":"<div><p><span><span><span>High altitude sickness is a life-threatening disease that occurs among acclimatized individuals working or living at a high altitude accompanied by hypobaric </span>hypoxia<span> exposure. The prolonged influence of hypobaric hypoxia on the brain may trigger neuronal damage and cell death due to an oxygen deficiency. The purpose of the current study was to investigate the histomorphological changes in the </span></span>hippocampus<span><span>, cerebral cortex, </span>cerebellar cortex, and striatum of the rat’s brain following chronic hypobaric hypoxia. Fourteen </span></span>albino rats<span><span> were used for this investigation. The animals were exposed to chronic hypobaric hypoxia in the special decompression chamber at an altitude of 7000 m for 7 days. The histological analysis was conducted via </span>toluidine<span><span><span> staining and silver impregnation. DNA damage and cell apoptosis were assessed via </span>Feulgen staining. The histochemical assessment revealed increased dark neurons in the hippocampus with cell swelling. Silver impregnation showed increased argyrophilic neurons in the cerebellar cortex, striatum, CA1 subfield of the hippocampus, and cerebral cortex. The cytochemical analysis determined the increased apoptotic cells with hyperchromatic condensation and </span>pyknosis in the hippocampus subfields and cerebral cortex. In addition, it has been observed that hypoxia has resulted in small hemorrhages and perivascular edema within the cerebellar and cerebral cortex.</span></span></p><p>The results indicate brain injury observed in the various parts of the brain towards hypobaric hypoxia, however, the hippocampus showed greater vulnerability against hypoxic exposure in comparison to the striatum, cerebellum, and cerebral cortex. These changes support our insights regarding brain intolerance under conditions of hypoxia-induced oxygen deficiency and its histomorphological manifestations.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"125 8","pages":"Article 152114"},"PeriodicalIF":2.5,"publicationDate":"2023-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136697190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Association between neuropeptides and mucins in Crohn’s disease mucous cells 克罗恩病黏液细胞中神经肽与黏液蛋白的关系
IF 2.5 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2023-11-17 DOI: 10.1016/j.acthis.2023.152115
Anthea Miller , Giuseppina Cutroneo , Giorgia Pia Lombardo , Roberta D’Angelo , Socrate Pallio , Alba Migliorato , Angelo Fumia , Angelo Favaloro , Eugenia Rita Lauriano , Simona Pergolizzi

Crohn’s disease (CD) and ulcerative colitis (UC) are both inflammatory bowel diseases (IBD). Unlike UC, which is limited to the mucosa of the colon, CD inflammation is characterized by chronic mucosal ulcerations affecting the entire gastrointestinal tract. Goblet cells (GCs) can be found in some lining epithelia, particularly in the respiratory and digestive tracts. GCs represent the main source of mucin that are the significant components of the mucus layer; hypertrophy of GCs and an increase in mucin production are observed in many enteric infections. The cytoplasm of goblet cells may also contain neuropeptides, such as serotonin, that can be altered in inflammatory bowel disease (IBD). The defense system of the gut is represented by the intestinal mucosal barrier, its protective function is strictly connected to the regulation of the mucus layer and the coordination of the neuro-immune response. Paraformaldehyde-fixed intestinal tissues, obtained from fifteen patients with Crohn’s disease, were analyzed by immunostaining for MUC2, MUC4, 5-HT, and VAChT. This study aims to define the link between neuropeptides and mucins in mucous cells and their involvement in the inflammation process. Our results showed in mucous cells of Crohn’s disease (CD) patients a high expression of MUC4 and a decrease in the expression of vesicular acetylcholine transporter (VAChT) demonstrating the presence of an inflammatory state.

克罗恩病(CD)和溃疡性结肠炎(UC)都是炎症性肠病(IBD)。与仅限于结肠粘膜的UC不同,CD炎症的特征是影响整个胃肠道的慢性粘膜溃疡。杯状细胞(GCs)可在某些粘膜上皮中发现,特别是在呼吸道和消化道中。GCs代表黏液蛋白的主要来源,是黏液层的重要组成部分;在许多肠道感染中观察到GCs的肥大和粘蛋白产生的增加。杯状细胞的细胞质也可能含有神经肽,如血清素,可在炎症性肠病(IBD)中发生改变。肠道的防御系统以肠黏膜屏障为代表,其保护功能与黏液层的调节和神经免疫反应的协调密切相关。对15例克罗恩病患者的多聚甲醛固定肠组织进行MUC2、MUC4、5-HT和VAChT的免疫染色分析。本研究旨在确定黏液细胞中神经肽和黏液蛋白之间的联系及其在炎症过程中的参与。我们的研究结果显示,在克罗恩病(CD)患者的粘膜细胞中MUC4的高表达和囊泡乙酰胆碱转运蛋白(VAChT)的表达减少,表明存在炎症状态。
{"title":"Association between neuropeptides and mucins in Crohn’s disease mucous cells","authors":"Anthea Miller ,&nbsp;Giuseppina Cutroneo ,&nbsp;Giorgia Pia Lombardo ,&nbsp;Roberta D’Angelo ,&nbsp;Socrate Pallio ,&nbsp;Alba Migliorato ,&nbsp;Angelo Fumia ,&nbsp;Angelo Favaloro ,&nbsp;Eugenia Rita Lauriano ,&nbsp;Simona Pergolizzi","doi":"10.1016/j.acthis.2023.152115","DOIUrl":"https://doi.org/10.1016/j.acthis.2023.152115","url":null,"abstract":"<div><p><span>Crohn’s disease (CD) and ulcerative colitis<span><span><span> (UC) are both inflammatory bowel diseases (IBD). Unlike UC, which is limited to the mucosa of the colon, CD inflammation is characterized by chronic mucosal </span>ulcerations<span> affecting the entire gastrointestinal tract. </span></span>Goblet cells (GCs) can be found in some lining epithelia, particularly in the respiratory and digestive tracts. GCs represent the main source of mucin that are the significant components of the </span></span>mucus<span><span><span> layer; hypertrophy of GCs and an increase in mucin production are observed in many enteric infections<span>. The cytoplasm of goblet cells may also contain neuropeptides, such as serotonin, that can be altered in inflammatory bowel disease (IBD). The defense system of the gut is represented by the </span></span>intestinal mucosal barrier<span>, its protective function is strictly connected to the regulation of the mucus layer and the coordination of the neuro-immune response. Paraformaldehyde-fixed intestinal tissues, obtained from fifteen patients with Crohn’s disease, were analyzed by immunostaining for </span></span>MUC2<span><span>, MUC4<span>, 5-HT, and VAChT. This study aims to define the link between neuropeptides and mucins in </span></span>mucous cells and their involvement in the inflammation process. Our results showed in mucous cells of Crohn’s disease (CD) patients a high expression of MUC4 and a decrease in the expression of vesicular acetylcholine transporter (VAChT) demonstrating the presence of an inflammatory state.</span></span></p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"125 8","pages":"Article 152115"},"PeriodicalIF":2.5,"publicationDate":"2023-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134832438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Immunolocalization of lix1 in the regenerating tail of lizard indicates that the protein is mainly present in the nervous tissue lix1在蜥蜴再生尾巴中的免疫定位表明该蛋白主要存在于神经组织中。
IF 2.5 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2023-11-08 DOI: 10.1016/j.acthis.2023.152113
Lorenzo Alibardi

Purpose

Lizard regeneration derives from the re-activation of a number of developmental genes after tail amputation. Among genes with the highest expression, as indicated from the transcriptome, is lix1 which functional role is not known.

Method

An antibody that cross-reacts with the lizard Podarcis muralis lix1 has been utilized to detect by immunofluorescence the sites of localization of the protein in the regenerating tail.

Results

Lix1-protein is almost exclusively localized in the regenerating spinal cord (ependyma) and nerves growing into the blastema, in sparse blastema cells but is undetectable in other tissues.

Conclusions

Since the spinal cord is essential to stimulate tail regeneration it is hypothesized that the lix1 protein is part of the signaling or growing factors produced from the regenerating spinal cord that are needed for tail regeneration of the lizard tail.

目的:蜥蜴的再生源于截肢后许多发育基因的重新激活。转录组显示,在表达最高的基因中,lix1的功能作用尚不清楚。方法:利用与蜥蜴Podarcis muralis lix1发生交叉反应的抗体,通过免疫荧光法检测再生尾巴中蛋白质的定位位点。结果:Lix1蛋白几乎完全定位于再生的脊髓(室管膜)和生长到芽基中的神经,在稀疏的芽基细胞中,但在其他组织中检测不到。结论:由于脊髓对刺激尾部再生至关重要,因此假设lix1蛋白是再生脊髓产生的信号传导或生长因子的一部分,这些因子是蜥蜴尾部再生所需的。
{"title":"Immunolocalization of lix1 in the regenerating tail of lizard indicates that the protein is mainly present in the nervous tissue","authors":"Lorenzo Alibardi","doi":"10.1016/j.acthis.2023.152113","DOIUrl":"10.1016/j.acthis.2023.152113","url":null,"abstract":"<div><h3>Purpose</h3><p>Lizard regeneration derives from the re-activation of a number of developmental genes after tail amputation. Among genes with the highest expression, as indicated from the transcriptome, is <em>lix1</em> which functional role is not known.</p></div><div><h3>Method</h3><p>An antibody that cross-reacts with the lizard <em>Podarcis muralis</em> lix1 has been utilized to detect by immunofluorescence the sites of localization of the protein in the regenerating tail.</p></div><div><h3>Results</h3><p>Lix1-protein is almost exclusively localized in the regenerating spinal cord (ependyma) and nerves growing into the blastema, in sparse blastema cells but is undetectable in other tissues.</p></div><div><h3>Conclusions</h3><p>Since the spinal cord is essential to stimulate tail regeneration it is hypothesized that the lix1 protein is part of the signaling or growing factors produced from the regenerating spinal cord that are needed for tail regeneration of the lizard tail.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"125 8","pages":"Article 152113"},"PeriodicalIF":2.5,"publicationDate":"2023-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72207930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Kisspeptin (Kp-10) inhibits in vitro osteogenic differentiation of multipotent mesenchymal stromal cells extracted from the bone marrow of adult rats Kisspeptin(Kp-10)抑制从成年大鼠骨髓中提取的多能间充质基质细胞的体外成骨分化。
IF 2.5 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2023-11-08 DOI: 10.1016/j.acthis.2023.152112
Laís Bitencourt Guimarães , Daniel Portela Dias Machado , Beatriz Ferreira Carvalho Versiani Caldeira , Larissa Tiemi Matuzake Vieira , Gabriela Alves Santos , Fabiana Rocha Araújo , Leonardo Teotônio Machado , Dawidson Assis Gomes , Natália de Melo Ocarino , Rogéria Serakides , Amanda Maria Sena Reis

Kisspeptin (Kp-10) is a neuropeptide that binds to GPR54 receptors, exerting several functions mainly in the nervous and reproductive systems of the body. However, its effects and mechanisms of action on the skeletal system remain poorly understood. This study evaluated the effects of different concentrations of Kp-10 on in vitro osteogenic differentiation of multipotent mesenchymal stromal cells (MSCs) extracted from the bone marrow (BM) of adult Wistar rats. Two-month-old female rats were euthanized to extract BM from long bones to obtain MSCs. Four experimental groups were established in vitro: a control and Kp-10 at concentrations of 0.01, 0.05 and, 0.1 µg/mL. After induction of osteogenic differentiation, cell viability was evaluated using the 3-(4,5-dimethylthiazol-2-yl)− 2,5-diphenyl tetrazolium bromide (MTT) assay, alkaline phosphatase activity, collagen synthesis, percentage of area covered by MSCs/field and mineralized nodules/field, and immunocytochemistry of the GPR54 receptor tests. Furthermore, evaluation of gene transcripts for type I collagen, Runx-2, Bmp-2, bone sialoprotein, osteocalcin and osteopontin was performed using real-time RT-qPCR. It was observed that MSCs expressed GPR54 receptor to which Kp-10 binds during osteogenic differentiation, promoting a negative effect on osteogenic differentiation. This effect was observed at all the Kp-10 concentrations in a concentration-dependent manner, characterized by a decrease in the activity of alkaline phosphatase, collagen synthesis, mineralized nodules, and decreased expression of gene transcripts for type I collagen, osteocalcin, osteopontin, and Runx-2. Thus, Kp-10 inhibits in vitro osteogenic differentiation of MSCs extracted from the BM of adult Wistar rats.

Kisspeptin(Kp-10)是一种与GPR54受体结合的神经肽,主要在身体的神经和生殖系统中发挥多种功能。然而,它对骨骼系统的影响和作用机制仍知之甚少。本研究评估了不同浓度的Kp-10对从成年Wistar大鼠骨髓(BM)中提取的多能间充质基质细胞(MSC)体外成骨分化的影响。对两个月大的雌性大鼠实施安乐死,从长骨中提取BM以获得MSC。在体外建立了四个实验组:对照组和浓度分别为0.01、0.05和0.1µg/mL的Kp-10。在诱导成骨分化后,使用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四氮唑(MTT)法、碱性磷酸酶活性、胶原合成,MSCs/field和矿化结节/field覆盖的面积百分比以及GPR54受体测试的免疫细胞化学。此外,使用实时RT-qPCR对I型胶原、Runx-2、Bmp-2、骨唾液蛋白、骨钙素和骨桥蛋白的基因转录物进行评估。观察到MSCs在成骨分化过程中表达GPR54受体,Kp-10与之结合,促进对成骨分化的负面影响。在所有Kp-10浓度下都以浓度依赖性的方式观察到这种作用,其特征是碱性磷酸酶、胶原合成、矿化结节的活性降低,以及I型胶原、骨钙素、骨桥蛋白和Runx-2的基因转录物的表达降低。因此,Kp-10抑制从成年Wistar大鼠的骨髓中提取的MSCs的体外成骨分化。
{"title":"Kisspeptin (Kp-10) inhibits in vitro osteogenic differentiation of multipotent mesenchymal stromal cells extracted from the bone marrow of adult rats","authors":"Laís Bitencourt Guimarães ,&nbsp;Daniel Portela Dias Machado ,&nbsp;Beatriz Ferreira Carvalho Versiani Caldeira ,&nbsp;Larissa Tiemi Matuzake Vieira ,&nbsp;Gabriela Alves Santos ,&nbsp;Fabiana Rocha Araújo ,&nbsp;Leonardo Teotônio Machado ,&nbsp;Dawidson Assis Gomes ,&nbsp;Natália de Melo Ocarino ,&nbsp;Rogéria Serakides ,&nbsp;Amanda Maria Sena Reis","doi":"10.1016/j.acthis.2023.152112","DOIUrl":"10.1016/j.acthis.2023.152112","url":null,"abstract":"<div><p>Kisspeptin (Kp-10) is a neuropeptide that binds to GPR54 receptors, exerting several functions mainly in the nervous and reproductive systems of the body. However, its effects and mechanisms of action on the skeletal system remain poorly understood. This study evaluated the effects of different concentrations of Kp-10 on <em>in vitr</em>o osteogenic differentiation of multipotent mesenchymal stromal cells (MSCs) extracted from the bone marrow (BM) of adult Wistar rats. Two-month-old female rats were euthanized to extract BM from long bones to obtain MSCs. Four experimental groups were established <em>in vitro</em>: a control and Kp-10 at concentrations of 0.01, 0.05 and, 0.1 µg/mL. After induction of osteogenic differentiation, cell viability was evaluated using the 3-(4,5-dimethylthiazol-2-yl)− 2,5-diphenyl tetrazolium bromide (MTT) assay, alkaline phosphatase activity, collagen synthesis, percentage of area covered by MSCs/field and mineralized nodules/field, and immunocytochemistry of the GPR54 receptor tests. Furthermore, evaluation of gene transcripts for type I collagen, <em>Runx-2</em>, Bmp-2<em>,</em> bone sialoprotein, osteocalcin and osteopontin was performed using real-time RT-qPCR. It was observed that MSCs expressed GPR54 receptor to which Kp-10 binds during osteogenic differentiation, promoting a negative effect on osteogenic differentiation. This effect was observed at all the Kp-10 concentrations in a concentration-dependent manner, characterized by a decrease in the activity of alkaline phosphatase, collagen synthesis, mineralized nodules, and decreased expression of gene transcripts for type I collagen, osteocalcin, osteopontin, and <em>Runx-2</em>. Thus, Kp-10 inhibits <em>in vitro</em> osteogenic differentiation of MSCs extracted from the BM of adult Wistar rats.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"125 8","pages":"Article 152112"},"PeriodicalIF":2.5,"publicationDate":"2023-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72207931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
In vitro validation: GLY alleviates UV-induced corneal epithelial damage through the HMGB1-TLR/MyD88-NF-κB signaling pathway 体外验证:GLY通过HMGB1-TLR/MyD88 NF-κB信号通路减轻紫外线诱导的角膜上皮损伤。
IF 2.5 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2023-11-06 DOI: 10.1016/j.acthis.2023.152111
XinYi Chen , XiaoXiao Zheng , Ting Shen , Ting He , YangQi Zhao , Yi Dong

UV-induced corneal damage is a common ocular surface injury that usually leads to corneal lesions causing persistent inflammation. High mobility group box 1 (HMGB1) is identified as an inflammatory alarm in various tissue injuries. Here, this study first evaluates the repair effect of the HMGB1-selective inhibitor GLY in UV-induced corneal damage; Secondly, the inhibitory effect of GLY on UV-induced corneal damage induced inflammation and the potential therapeutic mechanism of GLY were studied. GLY effectively attenuates the expression of UV-induced inflammatory factors and HMGB1, TLR/MyD88, NF-κB signaling pathway genes at the mRNA and protein levels. In addition, RT-PCR and Western Blot experiments after knocking down HMGB1 and TLR2/9 genes showed that GLY alleviated corneal inflammation by inhibiting the HMGB1-TLR/MyD88 signaling pathway. The results of this study show that targeting HMGB1-NF-κB by GLY can alleviate the inflammatory response induced by UV induction.

紫外线诱导的角膜损伤是一种常见的眼表损伤,通常会导致角膜损伤,引起持续的炎症。高迁移率组盒1(HMGB1)被确定为各种组织损伤中的炎症警报。在此,本研究首先评估了HMGB1选择性抑制剂GLY对紫外线诱导的角膜损伤的修复作用;其次,研究了GLY对紫外线诱导的角膜损伤诱导的炎症的抑制作用及其潜在的治疗机制。GLY在mRNA和蛋白质水平上有效减弱紫外线诱导的炎症因子和HMGB1、TLR/MyD88、NF-κB信号通路基因的表达。此外,敲低HMGB1和TLR2/9基因后的RT-PCR和Western Blot实验表明,GLY通过抑制HMGB1-TLR/MyD88信号通路来减轻角膜炎症。本研究结果表明,GLY靶向HMGB1-NF-κB可以减轻紫外线诱导的炎症反应。
{"title":"In vitro validation: GLY alleviates UV-induced corneal epithelial damage through the HMGB1-TLR/MyD88-NF-κB signaling pathway","authors":"XinYi Chen ,&nbsp;XiaoXiao Zheng ,&nbsp;Ting Shen ,&nbsp;Ting He ,&nbsp;YangQi Zhao ,&nbsp;Yi Dong","doi":"10.1016/j.acthis.2023.152111","DOIUrl":"10.1016/j.acthis.2023.152111","url":null,"abstract":"<div><p>UV-induced corneal damage is a common ocular surface injury that usually leads to corneal lesions causing persistent inflammation. High mobility group box 1 (HMGB1) is identified as an inflammatory alarm in various tissue injuries. Here, this study first evaluates the repair effect of the HMGB1-selective inhibitor GLY in UV-induced corneal damage; Secondly, the inhibitory effect of GLY on UV-induced corneal damage induced inflammation and the potential therapeutic mechanism of GLY were studied. GLY effectively attenuates the expression of UV-induced inflammatory factors and HMGB1, TLR/MyD88, NF-κB signaling pathway genes at the mRNA and protein levels. In addition, RT-PCR and Western Blot experiments after knocking down HMGB1 and TLR2/9 genes showed that GLY alleviated corneal inflammation by inhibiting the HMGB1-TLR/MyD88 signaling pathway. The results of this study show that targeting HMGB1-NF-κB by GLY can alleviate the inflammatory response induced by UV induction.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"125 8","pages":"Article 152111"},"PeriodicalIF":2.5,"publicationDate":"2023-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71520158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The effect on m6A methylation writer complex by the reduced MATR3 in pterygium 减少基质基质3对翼状胬肉中m6A甲基化复合物的影响
IF 2.5 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2023-10-31 DOI: 10.1016/j.acthis.2023.152101
Qianqian Guo, Shichao Han

Pterygium is a common eye surface disease with high recurrence and unclear pathogenesis. In current study, RNA sequencing was conducted in 6 pairs of human pterygium and conjunctival tissues, and Matr3 as a novel candidate gene was significantly reduced in pterygium compared to control tissues. Moreover, immunoprecipitation was performed to pull down MATR3, and WTAP specially interacting with MATR3 in control but not pterygium was identified by mass spectrum. Immunoprecipitation was performed to validate the interaction between MATR3 and WTAP/METTL3/METTL14 complex. (Methylated) RNA immunoprecipitation was performed to further reveal that the binding affinity of WTAP and MATR3 was lost at 3′ UTR of RNA molecules of down-regulated genes in pterygium. Overall, we figured out the loss of intercrossing between MATR3 and N6-methyladenosine methyltransferase complex, as well as indicated the potential impact on transcription of target genes in pterygium.

翼状胬肉是一种常见的眼表疾病,复发率高,发病机制不明确。本研究对6对人翼状胬肉和结膜组织进行了RNA测序,发现mat3作为一种新的候选基因在翼状胬肉中较对照组织明显减少。免疫沉淀法拉下mat3,质谱鉴定WTAP在对照中与mat3特异性相互作用,而在胬肉中不与mat3相互作用。免疫沉淀法验证了mat3与WTAP/METTL3/METTL14复合物之间的相互作用。(甲基化)RNA免疫沉淀进一步揭示WTAP与mat3的结合亲和力在翼状胬肉中下调基因的RNA分子的3 ' UTR处丢失。总的来说,我们发现了mat3与n6 -甲基腺苷甲基转移酶复合物之间的交叉缺失,并指出了对翼状胬肉靶基因转录的潜在影响。
{"title":"The effect on m6A methylation writer complex by the reduced MATR3 in pterygium","authors":"Qianqian Guo,&nbsp;Shichao Han","doi":"10.1016/j.acthis.2023.152101","DOIUrl":"https://doi.org/10.1016/j.acthis.2023.152101","url":null,"abstract":"<div><p><span><span>Pterygium is a common eye surface disease with high recurrence and unclear pathogenesis. In current study, </span>RNA sequencing was conducted in 6 pairs of human pterygium and conjunctival tissues, and </span><em>Matr3</em><span><span><span> as a novel candidate gene was significantly reduced in pterygium compared to control tissues. Moreover, immunoprecipitation was performed to pull down MATR3, and WTAP specially interacting with MATR3 in control but not pterygium was identified by mass spectrum. Immunoprecipitation was performed to validate the interaction between MATR3 and WTAP/METTL3/METTL14 complex. (Methylated) </span>RNA<span> immunoprecipitation was performed to further reveal that the binding affinity of WTAP and MATR3 was lost at 3′ UTR of RNA molecules of down-regulated genes in pterygium. Overall, we figured out the loss of intercrossing between MATR3 and N6-methyladenosine </span></span>methyltransferase complex, as well as indicated the potential impact on transcription of target genes in pterygium.</span></p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"125 8","pages":"Article 152101"},"PeriodicalIF":2.5,"publicationDate":"2023-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91991208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
MiR-223–3p overexpressed adipose mesenchymal stem cell-derived exosomes promote wound healing via targeting MAPK10 MiR-223-3p过表达的脂肪间充质干细胞衍生的外泌体通过靶向MAPK10促进伤口愈合。
IF 2.5 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2023-10-12 DOI: 10.1016/j.acthis.2023.152102
Xiaojiao Liu , Shunqiao Jin , Jiao Liu , Xuezhu Xu

Background

Adipose mesenchymal stem cell (AMSC)-derived exosomes are promising novel factors for wound repair and regeneration. This study aimed to explore the potential roles and underlying mechanisms of specific miRNA in wound healing using AMSC-derived exosomes as carriers.

Methods

The expression profiles of GSE197840 were downloaded to screen for differentially expressed miRNAs (DEmiRNAs), and the corresponding genes of the identified miRNAs were predicted. Next, miRNA-mRNA co-expression networks were constructed and the genes in these networks were subjected to functional analysis. miR-223–3p overexpressed AMSCs were then established to isolate exosomes, and the effects of AMSC-derived exosomes carrying miR-223–3p on wound healing and the related potential mechanisms were further investigated in vivo.

Results

35 DEmiRNAs were identified and a co-expression network containing 22 miRNAs and 91 target genes was constructed. Based on the network, miR-223–3p was the hub node and the genes were significantly enriched in 15 GO terms of biological processes and 14 KEGG pathways, including cAMP, PI3K-Akt, cGMP-PKG, neurotrophin signaling pathway, and dopaminergic synapse. Then, miR-223–3p overexpressed AMSCs-derived exosomes were successfully extracted, and miR-223–3p was found to directly bind with MAPK10. In vivo experiments validated that AMSCs-derived exosomal miR-223–3p could promote wound healing, and up-regulated α-SMA, CD31, COL1A1, COL2A1, COL3A1, and down-regulated MAPK10, TNF-α, IL-β, and IL-6.

Conclusions

AMSC-derived exosomal miR-223–3p may accelerate wound healing by targeting MAPK10.

背景:脂肪间充质干细胞(AMSC)来源的外泌体是一种很有前途的伤口修复和再生的新因子。本研究旨在利用AMSC衍生的外泌体作为载体,探索特异性miRNA在伤口愈合中的潜在作用和潜在机制。方法:下载GSE197840的表达谱以筛选差异表达的miRNA(DEmiRNA),并预测所鉴定的miRNA的相应基因。接下来,构建miRNA-mRNA共表达网络,并对这些网络中的基因进行功能分析。然后建立miR-223-3p过表达的AMSC来分离外泌体,并在体内进一步研究携带miR-223-3p的AMSC衍生的外泌体对伤口愈合的影响和相关的潜在机制。结果:共鉴定出35个DEmiRNA,构建了包含22个miRNA和91个靶基因的共表达网络。基于该网络,miR-223-3p是枢纽节点,这些基因在15个GO生物学过程和14个KEGG途径中显著富集,包括cAMP、PI3K-Akt、cGMP-PKG、神经营养因子信号通路和多巴胺能突触。然后,成功提取了miR-223-3p过表达的AMSCs衍生的外泌体,并发现miR-223-3p与MAPK10直接结合。体内实验证实,AMSC衍生的外泌体miR-223-3p可促进伤口愈合,上调α-SMA、CD31、COL1A1、COL2A1、COL3A1,下调MAPK10、TNF-α、IL-1β和IL-6。
{"title":"MiR-223–3p overexpressed adipose mesenchymal stem cell-derived exosomes promote wound healing via targeting MAPK10","authors":"Xiaojiao Liu ,&nbsp;Shunqiao Jin ,&nbsp;Jiao Liu ,&nbsp;Xuezhu Xu","doi":"10.1016/j.acthis.2023.152102","DOIUrl":"10.1016/j.acthis.2023.152102","url":null,"abstract":"<div><h3>Background</h3><p><span>Adipose mesenchymal stem cell (AMSC)-derived exosomes are promising novel factors for wound repair and regeneration. This study aimed to explore the potential roles and underlying mechanisms of specific </span>miRNA in wound healing using AMSC-derived exosomes as carriers.</p></div><div><h3>Methods</h3><p>The expression profiles of GSE197840 were downloaded to screen for differentially expressed miRNAs (DEmiRNAs), and the corresponding genes of the identified miRNAs were predicted. Next, miRNA-mRNA co-expression networks were constructed and the genes in these networks were subjected to functional analysis. miR-223–3p overexpressed AMSCs were then established to isolate exosomes, and the effects of AMSC-derived exosomes carrying miR-223–3p on wound healing and the related potential mechanisms were further investigated in vivo.</p></div><div><h3>Results</h3><p><span><span><span>35 DEmiRNAs were identified and a co-expression network containing 22 miRNAs and 91 target genes was constructed. Based on the network, miR-223–3p was the hub node and the genes were significantly enriched in 15 GO terms of </span>biological processes and 14 KEGG pathways, including cAMP, PI3K-Akt, cGMP-PKG, </span>neurotrophin<span><span> signaling pathway, and </span>dopaminergic synapse. Then, miR-223–3p overexpressed AMSCs-derived exosomes were successfully extracted, and miR-223–3p was found to directly bind with </span></span><span><em>MAPK10</em></span>. <em>In vivo</em> experiments validated that AMSCs-derived exosomal miR-223–3p could promote wound healing, and up-regulated α-SMA, <span><em>CD31</em></span>, COL1A1, <em>COL2A1</em>, <em>COL3A1</em>, and down-regulated MAPK10, TNF-α, <em>IL-β</em>, and <em>IL-6</em>.</p></div><div><h3>Conclusions</h3><p>AMSC-derived exosomal miR-223–3p may accelerate wound healing by targeting MAPK10.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"125 8","pages":"Article 152102"},"PeriodicalIF":2.5,"publicationDate":"2023-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41187811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Saikosaponin-d regulates angiogenesis in idiopathic pulmonary fibrosis through angiopoietin/Tie-2 pathway Saikosaponin-d通过血管生成素/Tie-2途径调节特发性肺纤维化的血管生成。
IF 2.5 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2023-10-12 DOI: 10.1016/j.acthis.2023.152100
Yan Wu , Jun Zhang , Xintian Wang , Yuncong Xu , Jinxu Zheng

Objective

Idiopathic pulmonary fibrosis (IPF) is considered as a chronic interstitial lung disease with underlying mechanism of IPF remaining unclear, while there are no definitive treatment options. In recent years, scientists have gradually paid attention to the influence of angiogenesis on IPF. Because IPF is a progressive with microvascular remodeling disorder, scientists have postulated that angiogenesis may also be one of the initiating and contributing factors of the disease. Bupleurum is a common natural Chinese herbal medicine with antibacterial, anti-inflammatory, anti-tumor and other pharmacological effects. As the most important active monomer of Bupleurum, Saikosaponin-d (SSd) is a new discovery with anti-pulmonary fibrosis (PF) activity. This study attempts to investigate the role of SSd in the interference of PF through regulation of angiogenesis in IPF through Angiopoietin (Angpt) /Tie receptor 2 (Tie2) pathway.

Methods

Randomly, we allocated C57BL/6 mice into four groups (n = 20 in each group). Afterwards, establishment of IPF model was accomplished via intratracheal administration of bleomycin (BLM, 5 mg/kg), while corresponding drug intervention was given accordingly. On 3rd, 7th, 14th and 28th days after modeling, we performed histopathological examination through staining. Meanwhile, immunohistochemistry (IHC) of PF and the expression of related factors were observed, while Ang/Tie2 pathway was assessed by ELISA with the effect of SSd on angiogenesis related proteins in IPF being explored with IHC and Western Blot technique.

Results

Our results showed that SSd could reduce inflammation and PF levels in lung tissue of experimental mice, while levels of angiogenesis-related factors, namely Tie-2, Ang-1 and ANGPT2 (Ang-2), fibrosis- associated factors like Alpha-smooth muscle actin (α-SMA), collagen-I and hydroxyproline in SSd and dexamethasone (DXM) mice were significantly reduced at each time point compared to BLM (p < 0.01). Additionally, we discovered substantial decreased expressions of Ang-1, Ang-2, Tie-2, α-SMA and collagen-I at protein level in SSd and DXM mice at each time point compared to BLM (p < 0.05). Besides, insignificant differences were observed between SSd and DXM groups (p > 0.05).

Conclusion

This study has demonstrated that SSd could down-regulate the expression of ANG-1, Ang-2 and Tie2 in the Ang/Tie2 pathway, and may reduce lung inflammation and PF in BLM-induced mice via inhibition of angiogenesis.

目的:特发性肺纤维化(IPF)被认为是一种慢性间质性肺病,其潜在机制尚不清楚,但尚无明确的治疗方案。近年来,科学家们逐渐关注血管生成对IPF的影响。由于IPF是一种进行性微血管重塑障碍,科学家们推测血管生成也可能是该疾病的起始和促成因素之一。柴胡是一种常见的天然中草药,具有抗菌、抗炎、抗肿瘤等药理作用。柴胡皂苷-d(SSd)作为柴胡最重要的活性单体,是一种具有抗肺纤维化(PF)活性的新发现。本研究试图通过血管生成素(Angpt)/Tie受体2(Tie2)途径调节IPF中的血管生成,探讨SSd在PF干扰中的作用。方法:将C57BL/6小鼠随机分为4组(每组20只)。然后,通过气管内给予博莱霉素(BLM,5mg/kg)建立IPF模型,并给予相应的药物干预。在建模后第3、7、14和28天,我们通过染色进行组织病理学检查。同时,观察PF的免疫组织化学(IHC)和相关因子的表达,同时用ELISA法评估Ang/Tie2通路,并用IHC和Western Blot技术探讨SSd对IPF血管生成相关蛋白的影响。结果:SSd可降低实验小鼠肺组织炎症和PF水平,而血管生成相关因子Tie-2、Ang-1和ANGPT2(Ang-2)、纤维化相关因子α-平滑肌肌动蛋白(α-SMA)、,与BLM相比,SSd和地塞米松(DXM)小鼠的胶原I和羟脯氨酸在每个时间点都显著降低(p0.05)。结论:本研究表明,SSd可以下调ANG/Tie2通路中ANG-1、ANG-2和Tie2的表达,并可能通过抑制血管生成来减轻BLM诱导的小鼠的肺部炎症和PF。
{"title":"Saikosaponin-d regulates angiogenesis in idiopathic pulmonary fibrosis through angiopoietin/Tie-2 pathway","authors":"Yan Wu ,&nbsp;Jun Zhang ,&nbsp;Xintian Wang ,&nbsp;Yuncong Xu ,&nbsp;Jinxu Zheng","doi":"10.1016/j.acthis.2023.152100","DOIUrl":"10.1016/j.acthis.2023.152100","url":null,"abstract":"<div><h3>Objective</h3><p>Idiopathic pulmonary fibrosis (IPF) is considered as a chronic interstitial lung disease with underlying mechanism of IPF remaining unclear, while there are no definitive treatment options. In recent years, scientists have gradually paid attention to the influence of angiogenesis on IPF. Because IPF is a progressive with microvascular remodeling disorder, scientists have postulated that angiogenesis may also be one of the initiating and contributing factors of the disease. Bupleurum is a common natural Chinese herbal medicine with antibacterial, anti-inflammatory, anti-tumor and other pharmacological effects. As the most important active monomer of Bupleurum, Saikosaponin-d (SSd) is a new discovery with anti-pulmonary fibrosis (PF) activity. This study attempts to investigate the role of SSd in the interference of PF through regulation of angiogenesis in IPF through Angiopoietin (Angpt) /Tie receptor 2 (Tie2) pathway.</p></div><div><h3>Methods</h3><p>Randomly, we allocated C57BL/6 mice into four groups (n = 20 in each group). Afterwards, establishment of IPF model was accomplished via intratracheal administration of bleomycin (BLM, 5 mg/kg), while corresponding drug intervention was given accordingly. On 3rd, 7th, 14th and 28th days after modeling, we performed histopathological examination through staining. Meanwhile, immunohistochemistry (IHC) of PF and the expression of related factors were observed, while Ang/Tie2 pathway was assessed by ELISA with the effect of SSd on angiogenesis related proteins in IPF being explored with IHC and Western Blot technique.</p></div><div><h3>Results</h3><p>Our results showed that SSd could reduce inflammation and PF levels in lung tissue of experimental mice, while levels of angiogenesis-related factors, namely Tie-2, Ang-1 and ANGPT2 (Ang-2), fibrosis- associated factors like Alpha-smooth muscle actin (α-SMA), collagen-I and hydroxyproline in SSd and dexamethasone (DXM) mice were significantly reduced at each time point compared to BLM (p &lt; 0.01). Additionally, we discovered substantial decreased expressions of Ang-1, Ang-2, Tie-2, α-SMA and collagen-I at protein level in SSd and DXM mice at each time point compared to BLM (p &lt; 0.05). Besides, insignificant differences were observed between SSd and DXM groups (p &gt; 0.05).</p></div><div><h3>Conclusion</h3><p>This study has demonstrated that SSd could down-regulate the expression of ANG-1, Ang-2 and Tie2 in the Ang/Tie2 pathway, and may reduce lung inflammation and PF in BLM-induced mice via inhibition of angiogenesis.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"125 8","pages":"Article 152100"},"PeriodicalIF":2.5,"publicationDate":"2023-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41187812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Inhibitory effect of telocyte-induced M1 macrophages on endometriosis: Targeting angiogenesis and invasion 毛细血管细胞诱导的M1巨噬细胞对子宫内膜异位症的抑制作用:靶向血管生成和侵袭。
IF 2.5 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2023-10-07 DOI: 10.1016/j.acthis.2023.152099
Xiao-Jiao Wei , Yue-lin Huang , Tian-Quan Chen , Xiao-Jun Yang

Purpose

Telocytes (TCs), a novel type of stromal cells found in tissues, induce macrophage differentiation into classically activated macrophages (M1) types and enhance their phagocytic function. The purpose of this study was to investigate the inhibitory effects of TC-induced M1 macrophages on endometriosis (EMs).

Methods

mouse uterine primary TCs and endometrial stromal cells (ESCs) were isolated and identified using double immunofluorescence staining. For the in vitro study, ESCs were treated with TC-induced M1 macrophages, and the vascular endothelial growth factor (VEGF), matrix metalloproteinase 9 (MMP9), and nuclear factor kappa B (NF-κb) genes were identified by quantitative real-time PCR (qRT-PCR) or western blotting (WB). For the in vivo study, an EMs mouse model received TC-conditioned medium (TCM) via abdominal administration, and characterized the inhibitory effects on growth (lesion weight, volume, and pathology), tissue-resident macrophages differentiation by immunostaining, angiogenic capacity (CD31 and VEGF), invasive capacity (MMP9), and NF-κb expression within EMs lesions.

Results

immunofluorescent staining showed that uterine TCs expressed CD34+ and vimentin+, whereas ESCs expressed vimentin+ and cytokeratin-. At the cellular level, TC-induced M1 macrophages can significantly inhibit the expression of VEGF and MMP9 in ESCs through WB or qRT-PCR, possibly by suppressing the NF-κb pathway. The in vivo study showed that macrophages switch from the alternatively activated macrophages (M2) in untreated EMs lesions to the M1 subtype after TCM exposure. Thereby, TC-induced M1 macrophages contributed to the inhibition of EMs lesions. More importantly, this effect may be achieved by suppressing the expression of NF-κb to inhibit angiogenesis (CD31 and VEGF) and invasion (MMP9) in the tissue.

Conclusion

TC-induced M1 macrophages play a prevailing role in suppressing EMs by inhibiting angiogenic and invasive capacity through the NF-κb pathway, which provides a promising therapeutic approach for EMs.

目的:Telocytes(TC)是一种在组织中发现的新型基质细胞,可诱导巨噬细胞分化为经典活化的巨噬细胞(M1)类型,并增强其吞噬功能。本研究旨在探讨TC诱导的M1巨噬细胞对子宫内膜异位症(EM)的抑制作用。在体外研究中,用TC诱导的M1巨噬细胞处理ESCs,并通过实时定量PCR(qRT-PCR)或蛋白质印迹(WB)鉴定血管内皮生长因子(VEGF)、基质金属蛋白酶9(MMP9)和核因子κB(NF-κB)基因。在体内研究中,EM小鼠模型通过腹部给药接受TC条件培养基(TCM),并通过免疫染色、血管生成能力(CD31和VEGF)、侵袭能力(MMP9)和EM病变内NF-κb表达来表征对生长(病变重量、体积和病理学)、组织驻留巨噬细胞分化的抑制作用。结果:免疫荧光染色显示子宫TC表达CD34+和波形蛋白+,而ESCs表达波形蛋白和细胞角蛋白-。在细胞水平上,TC诱导的M1巨噬细胞可以通过WB或qRT-PCR显著抑制ESCs中VEGF和MMP9的表达,可能是通过抑制NF-κb途径。体内研究表明,在中药暴露后,巨噬细胞从未经治疗的EM病变中的选择性活化巨噬细胞(M2)转变为M1亚型。因此,TC诱导的M1巨噬细胞有助于抑制EMs损伤。更重要的是,这种作用可以通过抑制NF-κb的表达来抑制组织中的血管生成(CD31和VEGF)和侵袭(MMP9)来实现。结论:TC诱导的M1巨噬细胞通过NF-κb途径抑制血管生成和侵袭能力,在抑制EM中发挥重要作用,为EM的治疗提供了一种有前景的途径。
{"title":"Inhibitory effect of telocyte-induced M1 macrophages on endometriosis: Targeting angiogenesis and invasion","authors":"Xiao-Jiao Wei ,&nbsp;Yue-lin Huang ,&nbsp;Tian-Quan Chen ,&nbsp;Xiao-Jun Yang","doi":"10.1016/j.acthis.2023.152099","DOIUrl":"10.1016/j.acthis.2023.152099","url":null,"abstract":"<div><h3>Purpose</h3><p>Telocytes (TCs), a novel type of stromal cells found in tissues, induce macrophage differentiation into classically activated macrophages (M1) types and enhance their phagocytic function. The purpose of this study was to investigate the inhibitory effects of TC-induced M1 macrophages on endometriosis (EMs).</p></div><div><h3>Methods</h3><p>mouse uterine primary TCs and endometrial stromal cells (ESCs) were isolated and identified using double immunofluorescence staining. For the <em>in vitro</em> study, ESCs were treated with TC-induced M1 macrophages, and the vascular endothelial growth factor (<em>VEGF</em>), matrix metalloproteinase 9 (<em>MMP9</em>), and nuclear factor kappa B (<em>NF-κb</em>) genes were identified by quantitative real-time PCR (qRT-PCR) or western blotting (WB). For the <em>in vivo</em> study, an EMs mouse model received TC-conditioned medium (TCM) <em>via</em> abdominal administration, and characterized the inhibitory effects on growth (lesion weight, volume, and pathology), tissue-resident macrophages differentiation by immunostaining, angiogenic capacity (CD31 and VEGF), invasive capacity (MMP9), and NF-κb expression within EMs lesions.</p></div><div><h3>Results</h3><p>immunofluorescent staining showed that uterine TCs expressed CD34+ and vimentin+, whereas ESCs expressed vimentin+ and cytokeratin-. At the cellular level, TC-induced M1 macrophages can significantly inhibit the expression of VEGF and MMP9 in ESCs through WB or qRT-PCR, possibly by suppressing the NF-κb pathway. The <em>in vivo</em> study showed that macrophages switch from the alternatively activated macrophages (M2) in untreated EMs lesions to the M1 subtype after TCM exposure. Thereby, TC-induced M1 macrophages contributed to the inhibition of EMs lesions. More importantly, this effect may be achieved by suppressing the expression of NF-κb to inhibit angiogenesis (CD31 and VEGF) and invasion (MMP9) in the tissue.</p></div><div><h3>Conclusion</h3><p>TC-induced M1 macrophages play a prevailing role in suppressing EMs by inhibiting angiogenic and invasive capacity through the NF-κb pathway, which provides a promising therapeutic approach for EMs.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"125 8","pages":"Article 152099"},"PeriodicalIF":2.5,"publicationDate":"2023-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41181745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Acta histochemica
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1