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Corrigendum to “AARS1-mediated Osterix lactylation promotes its transcriptional activity during osteoblast differentiation” [Acta Histochem. 127 (2025) 152273] “aars1介导的Osterix乳酸化促进成骨细胞分化过程中的转录活性”的更正[Acta Histochem. 127(2025) 152273]。
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-06-23 DOI: 10.1016/j.acthis.2025.152275
Feige Nian , Linfeng Guo , Zhangli Fei , Mingfeng Yang , Lihong Chen , Ye Zhang , Zhufeng Zhang , Yezhou Qian , Bin Zhang
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引用次数: 0
Calcipotriol inhibits the proliferation of psoriasis HaCaT cells by activating the ferroptosis pathway 钙化三醇通过激活铁下垂途径抑制银屑病HaCaT细胞的增殖
IF 2.3 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-06-23 DOI: 10.1016/j.acthis.2025.152274
Lei Yang , Yue Zhang , Jiansong Wu , Lei Wang , Shan Liu , Li Zhou , Jigang Zhang , Chengxin Li
Calcipotriol is a well-established treatment for psoriasis and other dermatological conditions. This study aimed to investigate whether calcipotriol exerts its therapeutic effects through ferroptosis and to elucidate its underlying molecular mechanisms using bioinformatics and cellular experiments. Differentially expressed genes (DEGs) and their functional enrichment were analyzed in psoriatic skin lesions using bioinformatics. A lipopolysaccharide (LPS)-induced HaCaT cell model was established to simulate psoriatic inflammation. The effects of calcipotriol at various concentrations and time points on HaCaT cell proliferation, apoptosis, and expression of key markers were assessed. Additionally, ferrostatin-1 (a ferroptosis inhibitor) and RSL3 (a ferroptosis inducer) were used to evaluate ferroptosis-related changes, including cell proliferation, apoptosis, reactive oxygen species (ROS) levels, glutathione (GSH) content (via ELISA), and protein expression of GPX4 and Ki-67 (via Western blot). Bioinformatics analysis revealed significant differential expression of ferroptosis-related genes, such as GPX4 and SLC7A11, in psoriatic lesions. Calcipotriol treatment inhibited HaCaT cell proliferation in a dose- and time-dependent manner, elevated ROS levels, and reduced GSH, GPX4, and Ki-67 expression. These effects were reversed by ferrostatin-1, which restored antioxidant defenses and cell viability. Conversely, RSL3 increased ROS levels and partially negated the protective effects of ferrostatin-1. These findings suggest that calcipotriol regulates ferroptosis-related gene expression and inhibits keratinocyte proliferation through induction of oxidative stress and ferroptosis, offering new insights into its mechanism of action in psoriasis treatment.
钙化三醇是治疗牛皮癣和其他皮肤病的有效方法。本研究旨在通过生物信息学和细胞实验研究钙化三醇是否通过铁下垂发挥其治疗作用,并阐明其潜在的分子机制。应用生物信息学方法对银屑病皮损中的差异表达基因(DEGs)及其功能富集进行了分析。建立脂多糖(LPS)诱导HaCaT细胞模型,模拟银屑病炎症。观察不同浓度、不同时间点钙三醇对HaCaT细胞增殖、凋亡及关键标志物表达的影响。此外,利用铁抑素-1(一种铁下垂抑制剂)和RSL3(一种铁下垂诱诱剂)评估铁下垂相关的变化,包括细胞增殖、凋亡、活性氧(ROS)水平、谷胱甘肽(GSH)含量(通过ELISA)以及GPX4和Ki-67的蛋白表达(通过Western blot)。生物信息学分析显示,银屑病皮损中与铁中毒相关的基因GPX4和SLC7A11的表达存在显著差异。钙化三醇以剂量和时间依赖性的方式抑制HaCaT细胞增殖,升高ROS水平,降低GSH、GPX4和Ki-67的表达。这些作用被铁他汀-1逆转,恢复抗氧化防御和细胞活力。相反,RSL3增加ROS水平,部分抵消了铁stat -1的保护作用。这些发现提示钙化三醇通过诱导氧化应激和铁下垂调节铁中毒相关基因表达,抑制角化细胞增殖,为其治疗银屑病的作用机制提供了新的见解。
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引用次数: 0
AARS1-mediated Osterix lactylation promotes its transcriptional activity during osteoblast differentiation aars1介导的Osterix乳酸化在成骨细胞分化过程中促进其转录活性
IF 2.3 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-06-11 DOI: 10.1016/j.acthis.2025.152273
Feige Nian , Linfeng Guo , Zhangli Fei , Mingfeng Yang , Lihong Chen , Ye Zhang , Bin Zhang , Yezhou Qian , Zhufeng Zhang
AARS1 is a newly reported lactyl-transferase that plays vital roles in tumorigenesis and innate immune response. However, the function of AARS1-mediated lactylation in osteoblast differentiation is still unclear. Here, we found that silencing of AARS1 impaired the ALP activity and formation of mineralized nodules during osteoblast differentiation. Additionally, our findings demonstrated that AARS1 catalyzed lactylation of Osterix (Osx), a crucial transcription factor involved in the differentiation process of osteoblast cells. Lactylation of Osx increased its binding to target genes and promoted the interaction between Osx and WDR5, facilitating H3K4 tri-methylation on downstream target genes. This in turn enhanced the expression of Osx target genes and osteoblast differentiation. In summary, our study revealed a novel role of AARS1-mediated Osx lactylation during osteoblast differentiation.
AARS1是一种新报道的乙酰转移酶,在肿瘤发生和先天免疫反应中起重要作用。然而,aars1介导的乳酸化在成骨细胞分化中的作用尚不清楚。我们发现,在成骨细胞分化过程中,AARS1的沉默会损害ALP活性和矿化结节的形成。此外,我们的研究结果表明,AARS1催化Osterix (Osx)的乳酸化,Osterix是参与成骨细胞分化过程的关键转录因子。Osx的乳酸化增加了其与靶基因的结合,促进了Osx与WDR5的相互作用,促进了下游靶基因上H3K4的三甲基化。这反过来又增强了Osx靶基因的表达和成骨细胞的分化。总之,我们的研究揭示了aars1介导的Osx乳酸化在成骨细胞分化中的新作用。
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引用次数: 0
Retraction notice to “Targeting TEAD would be a potential strategy for scarless wound repair: A preliminary study" [ Acta Histochem. 127 (2025), 152223] “靶向TEAD可能是无疤痕伤口修复的潜在策略:一项初步研究”[Acta Histochem. 127(2025), 152223]。
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-06-10 DOI: 10.1016/j.acthis.2025.152271
Ming-Yan Yang , Hong-Yuan Quan , Da-Lei Li , Jian Ruan , Hua-Ying Fan
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引用次数: 0
Characterization of immune cells in the rat intestinal mucosa and liver involved in inflammation caused by LPS and evaluation of the effects of N-acetylcysteine and disulfiram (well-known sulfur drugs) for this inflammation LPS引起的大鼠肠黏膜和肝脏炎症中免疫细胞的特征及n -乙酰半胱氨酸和双硫仑(众所周知的含硫药物)对这种炎症的作用的评价
IF 2.3 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-06-06 DOI: 10.1016/j.acthis.2025.152272
Anthea Miller , Giorgia Pia Lombardo , Laura Spiccia , Valentina Natale , Alba Migliorato , Marek Bednarski , Małgorzata Iciek , Anna Bilska-Wilkosz , Mateusz Sablik , Eugenia Rita Lauriano , Magdalena Kotańska , Simona Pergolizzi
Lipopolysaccharide (LPS)-induced inflammation is an experimental rat model often used as a tool for testing new drugs as candidates for treating various diseases associated with inflammation. New methods now allow for precise imaging of tissues and changes induced by various factors. To increase knowledge about LPS-induced inflammation and promote strategies for investigating new therapies, this study aims to characterize immune cells involved in inflammation in the rat intestinal mucosa and liver and to evaluate the therapeutic effect of two well-known sulfur drugs N-acetylcysteine (NAC) and disulfiram (DSF) on this model LPS was administered intraperitoneally to rats once a day, for 10 days. NAC and DSF were administered 5 h after LPS. At the end of experiment, animals were euthanized, and the intestine and liver were collected. The immune cells of the intestinal mucosa and liver were characterized with the following antibodies: Toll-like receptors (TLR2 and TLR4), smooth muscle alpha-actin (α-SMA), major histocompatibility complex II (MHC-II), and serotonin (5-HT). In samples obtained from inflamed rat intestinal mucosa, it was possible to detect TLR2-positive and TLR4-positive cells, and numerous α-SMA-positive cells, indicating an inflammatory state. Furthermore, an increase in serotonin positive neuroendocrine cells compared to normal was demonstrated, which could be associated with intestinal inflammation. The number of these positive cells was much smaller in the samples derived from animals treated with NAC or DSF, suggesting anti-inflammatory action of these drugs. In the inflamed rat liver, several immune cells positive for these antibodies were observed and NAC or DSF decreased the amount of these positive cells. In conclusion, this study shows that bacterial LPS can activate various innate immune system cell populations, such as dendritic cells, neutrophils, Kupffer cells, myofibroblasts and enterocytes. Moreover, this study demonstrates the beneficial effects on NAC and DSF in alleviating inflammation and relieving tissue fibrosis in the LPS-induced inflammation in the rat intestinal mucosa and liver.
脂多糖(LPS)诱导的炎症是一种实验性大鼠模型,经常被用作测试新药作为治疗各种炎症相关疾病的候选药物的工具。现在的新方法允许对组织和由各种因素引起的变化进行精确成像。为了增加对脂多糖诱导炎症的认识,促进研究新疗法的策略,本研究旨在表征大鼠肠黏膜和肝脏中参与炎症的免疫细胞,并评估两种著名的硫药物n -乙酰半胱氨酸(NAC)和双硫仑(DSF)对该模型的治疗效果,LPS每天腹腔注射一次,持续10天。LPS后5 h给予NAC和DSF。实验结束时,对动物实施安乐死,取肠、肝。肠黏膜和肝脏免疫细胞的主要抗体为toll样受体(TLR2和TLR4)、平滑肌α-肌动蛋白(α-SMA)、主要组织相容性复合体II (MHC-II)和血清素(5-HT)。在炎症大鼠肠黏膜样品中,可以检测到tlr2阳性和tlr4阳性细胞,以及大量α- sma阳性细胞,表明炎症状态。此外,与正常相比,血清素阳性神经内分泌细胞增加,这可能与肠道炎症有关。在NAC或DSF处理的动物样本中,这些阳性细胞的数量要少得多,这表明这些药物具有抗炎作用。在炎症大鼠肝脏中,观察到一些免疫细胞对这些抗体呈阳性,NAC或DSF减少了这些阳性细胞的数量。综上所述,本研究表明细菌LPS可以激活多种先天免疫系统细胞群,如树突状细胞、中性粒细胞、库普弗细胞、肌成纤维细胞和肠细胞。此外,本研究还证实了NAC和DSF在lps诱导的大鼠肠黏膜和肝脏炎症中具有减轻炎症和缓解组织纤维化的有益作用。
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引用次数: 0
Exosomal delivery of AZD5582 to overcome TRAIL resistance as an optimal therapy against triple-negative breast cancer 外泌体递送AZD5582克服TRAIL耐药是治疗三阴性乳腺癌的最佳方法
IF 2.3 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-05-24 DOI: 10.1016/j.acthis.2025.152270
Wanting Zhang , Quanjiang Li , Rui Tian , Zhujie Deng , Ronghui Sun , Xiubin Kuang , Jun Peng , Bin Xie , Chen Huang , Zhengqiang Yuan
Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer that lacks effective targeted therapies mainly due to drug resistance. Therefore, there is an urgent need to develop highly effective therapeutic strategies for TNBC. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis in transformed and cancerous cells, indicating its potential for anti-cancer therapy. Unfortunately, the clinical trials of recombinant TRAIL (rTRAIL) had actually failed due to the very common TRAIL resistance in cancers. Exosomal delivery of TRAIL (EV-T) has been shown to greatly improve the cytotoxicity of TRAIL. Moreover, the TRAIL resistance was closely correlated with the upregulation of inhibitors of apoptosis proteins (IAPs) in cancer cells. As a potent antagonist of IAPs, AZD5582 (AZD) was previously shown to drastically sensitize TRAIL response. Herein, we hypothesize that AZD may be loaded into EV-T for co-delivery of AZD and TRAIL to make a synergistic combination anticancer therapy against TNBC. First, TRAIL-expressing mesenchymal stem cells (MSCs) were used to prepare EV-Ts. Then, AZD was loaded into EV-T by ultrasound to prepare the composite nanodrug AZD@EV-T. EV encapsulation significantly improved AZD stability and cellular delivery efficiency, leading to the synergistically augmented cytotoxicity and apoptosis induction in both breast and kidney cancer cell lines, whilst sparing the normal MSCs. The potential mechanisms underlying the synergism appeared to be associated with the concomitant upregulation of death receptor 5 (DR5) and expressional suppression of various anti-apoptotic factors. Importantly, the AZD@EV-T therapy triggered strikingly enhanced growth inhibition and apoptosis in the subcutaneously established BT549 xenograft tumors, consequently leading to the complete tumor regression. It also demonstrated significant potential for treating kidney cancer in A498 kidney tumor organoids. Together, AZD@EV-T effectively overcomes TRAIL resistance and may represent a highly effective and innovative anticancer therapy for both TNBC and kidney cancers.
三阴性乳腺癌(TNBC)是一种高度侵袭性的乳腺癌亚型,主要由于耐药而缺乏有效的靶向治疗。因此,迫切需要开发高效的TNBC治疗策略。肿瘤坏死因子(Tumor necrosis factor, TNF)相关凋亡诱导配体(apoptosis-inducing ligand, TRAIL)在转化细胞和癌细胞中选择性诱导凋亡,表明其具有抗癌治疗的潜力。不幸的是,重组TRAIL (rTRAIL)的临床试验实际上失败了,因为TRAIL在癌症中非常常见。外泌体递送TRAIL (EV-T)已被证明可大大改善TRAIL的细胞毒性。此外,TRAIL耐药与癌细胞中凋亡蛋白抑制剂(IAPs)的上调密切相关。作为一种有效的IAPs拮抗剂,AZD5582 (AZD)先前被证明能显著致敏TRAIL反应。在此,我们假设AZD可能被装载到EV-T中,共同递送AZD和TRAIL,从而形成针对TNBC的协同联合抗癌治疗。首先,利用表达trail的间充质干细胞(MSCs)制备EV-Ts。然后,通过超声将AZD加载到EV-T中,制备复合纳米药物AZD@EV-T。EV包封显著提高了AZD的稳定性和细胞递送效率,从而协同增强了乳腺癌和肾癌细胞系的细胞毒性和凋亡诱导,同时保留了正常的MSCs。协同作用的潜在机制似乎与死亡受体5 (DR5)的上调和各种抗凋亡因子的表达抑制有关。重要的是,AZD@EV-T治疗在皮下建立的BT549异种移植肿瘤中引发了显著增强的生长抑制和细胞凋亡,从而导致肿瘤完全消退。在A498肾肿瘤类器官中也显示出治疗肾癌的显著潜力。总之,AZD@EV-T有效地克服了TRAIL耐药性,可能代表了TNBC和肾癌的一种高效和创新的抗癌疗法。
{"title":"Exosomal delivery of AZD5582 to overcome TRAIL resistance as an optimal therapy against triple-negative breast cancer","authors":"Wanting Zhang ,&nbsp;Quanjiang Li ,&nbsp;Rui Tian ,&nbsp;Zhujie Deng ,&nbsp;Ronghui Sun ,&nbsp;Xiubin Kuang ,&nbsp;Jun Peng ,&nbsp;Bin Xie ,&nbsp;Chen Huang ,&nbsp;Zhengqiang Yuan","doi":"10.1016/j.acthis.2025.152270","DOIUrl":"10.1016/j.acthis.2025.152270","url":null,"abstract":"<div><div>Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer that lacks effective targeted therapies mainly due to drug resistance. Therefore, there is an urgent need to develop highly effective therapeutic strategies for TNBC. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis in transformed and cancerous cells, indicating its potential for anti-cancer therapy. Unfortunately, the clinical trials of recombinant TRAIL (rTRAIL) had actually failed due to the very common TRAIL resistance in cancers. Exosomal delivery of TRAIL (EV-T) has been shown to greatly improve the cytotoxicity of TRAIL. Moreover, the TRAIL resistance was closely correlated with the upregulation of inhibitors of apoptosis proteins (IAPs) in cancer cells. As a potent antagonist of IAPs, AZD5582 (AZD) was previously shown to drastically sensitize TRAIL response. Herein, we hypothesize that AZD may be loaded into EV-T for co-delivery of AZD and TRAIL to make a synergistic combination anticancer therapy against TNBC. First, TRAIL-expressing mesenchymal stem cells (MSCs) were used to prepare EV-Ts. Then, AZD was loaded into EV-T by ultrasound to prepare the composite nanodrug AZD@EV-T. EV encapsulation significantly improved AZD stability and cellular delivery efficiency, leading to the synergistically augmented cytotoxicity and apoptosis induction in both breast and kidney cancer cell lines, whilst sparing the normal MSCs. The potential mechanisms underlying the synergism appeared to be associated with the concomitant upregulation of death receptor 5 (DR5) and expressional suppression of various anti-apoptotic factors. Importantly, the AZD@EV-T therapy triggered strikingly enhanced growth inhibition and apoptosis in the subcutaneously established BT549 xenograft tumors, consequently leading to the complete tumor regression. It also demonstrated significant potential for treating kidney cancer in A498 kidney tumor organoids. Together, AZD@EV-T effectively overcomes TRAIL resistance and may represent a highly effective and innovative anticancer therapy for both TNBC and kidney cancers.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"127 3","pages":"Article 152270"},"PeriodicalIF":2.3,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144131386","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
Lysophosphatidic acid (LPA) receptor signaling enhances malignant potential in highly migratory lung cancer cells under hypoxic conditions 溶血磷脂酸(LPA)受体信号在缺氧条件下增强高迁移肺癌细胞的恶性潜能
IF 2.3 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-05-23 DOI: 10.1016/j.acthis.2025.152268
Moemi Tamura, Miwa Takai, Mao Yamamoto, Narumi Yashiro, Anri Taniguchi, Yuka Kusumoto, Shion Nagano, Nanami Shimomura, Toshifumi Tsujiuchi
Hypoxia contributes to tumor progression, promoting cancer cell motility, invasion and metastasis. Lysophosphatidic acid (LPA) receptors are implicated in the pathogenesis of cancer. In this study, we investigated the role of LPA receptor signaling in modulating malignant behavior under hypoxic conditions (1 % O2) in lung cancer cells. We generated highly migratory A549-R12 cells from the parental lung cancer A549 cells for this purpose. LPAR1 and LPAR2 expression levels were lower in both A549 and A549-R12 cells cultured at 1 % O2 compared to those cultured at 21 % O2, while LPAR3 expression remained unchanged between the two cell lines. Cell motility increased in both A549 and A549-R12 cells cultured at 1 % O2. Notably, A549-R12 cells exhibited greater motility under 1 % O2 conditions than A549 cells. Treatment with AM966 (an LPA1 antagonist) and (2S)-OMPT (an LPA3 agonist) further increased the motility of A549-R12 cells, while GRI-977143 (an LPA2 agonist) decreased their motility. Moreover, the invasion activity of A549-R12 cells was higher than that of A549 cells, with 1 % O2 conditions significantly enhancing A549-R12 cell invasion. AM966 and (2S)-OMPT stimulated, whereas GRI-977143 inhibited, the invasion of A549-R12 cells. In the presence of LPA, cell viability to cisplatin (CDDP) was higher in A549-R12 cells cultured at both 21 % and 1 % O2 compared to A549 cells. These results suggest that LPA receptor signaling plays a key role in regulating malignant progression in highly migratory lung cancer cells under hypoxic conditions.
缺氧有助于肿瘤的进展,促进癌细胞的运动、侵袭和转移。溶血磷脂酸(LPA)受体与癌症的发病机制有关。在这项研究中,我们研究了LPA受体信号在低氧条件下(1 % O2)在肺癌细胞中调节恶性行为的作用。为此,我们从亲代肺癌A549细胞中产生了高度迁移的A549- r12细胞。在1 % O2下培养的A549和A549- r12细胞中,LPAR1和LPAR2的表达水平低于在21 % O2下培养的细胞,而LPAR3的表达在两种细胞系之间保持不变。在1 % O2条件下培养的A549和A549- r12细胞的细胞活力均增加。值得注意的是,A549- r12细胞在1 % O2条件下比A549细胞表现出更大的运动性。AM966 (LPA1拮抗剂)和(2S)-OMPT (LPA3激动剂)进一步增加了A549-R12细胞的运动性,而GRI-977143 (LPA2激动剂)降低了它们的运动性。此外,A549- r12细胞的侵袭活性高于A549细胞,1 % O2条件显著增强A549- r12细胞的侵袭活性。AM966和(2S)-OMPT刺激A549-R12细胞的侵袭,而GRI-977143抑制A549-R12细胞的侵袭。在LPA存在的情况下,与A549细胞相比,在21 %和1 % O2下培养的A549- r12细胞对顺铂(CDDP)的存活率更高。这些结果表明LPA受体信号在缺氧条件下调节高迁移性肺癌细胞的恶性进展中起关键作用。
{"title":"Lysophosphatidic acid (LPA) receptor signaling enhances malignant potential in highly migratory lung cancer cells under hypoxic conditions","authors":"Moemi Tamura,&nbsp;Miwa Takai,&nbsp;Mao Yamamoto,&nbsp;Narumi Yashiro,&nbsp;Anri Taniguchi,&nbsp;Yuka Kusumoto,&nbsp;Shion Nagano,&nbsp;Nanami Shimomura,&nbsp;Toshifumi Tsujiuchi","doi":"10.1016/j.acthis.2025.152268","DOIUrl":"10.1016/j.acthis.2025.152268","url":null,"abstract":"<div><div>Hypoxia contributes to tumor progression, promoting cancer cell motility, invasion and metastasis. Lysophosphatidic acid (LPA) receptors are implicated in the pathogenesis of cancer. In this study, we investigated the role of LPA receptor signaling in modulating malignant behavior under hypoxic conditions (1 % O<sub>2</sub>) in lung cancer cells. We generated highly migratory A549-R12 cells from the parental lung cancer A549 cells for this purpose. <em>LPAR1</em> and <em>LPAR2</em> expression levels were lower in both A549 and A549-R12 cells cultured at 1 % O<sub>2</sub> compared to those cultured at 21 % O<sub>2</sub>, while <em>LPAR3</em> expression remained unchanged between the two cell lines. Cell motility increased in both A549 and A549-R12 cells cultured at 1 % O<sub>2</sub>. Notably, A549-R12 cells exhibited greater motility under 1 % O<sub>2</sub> conditions than A549 cells. Treatment with AM966 (an LPA<sub>1</sub> antagonist) and (2S)-OMPT (an LPA<sub>3</sub> agonist) further increased the motility of A549-R12 cells, while GRI-977143 (an LPA<sub>2</sub> agonist) decreased their motility. Moreover, the invasion activity of A549-R12 cells was higher than that of A549 cells, with 1 % O<sub>2</sub> conditions significantly enhancing A549-R12 cell invasion. AM966 and (2S)-OMPT stimulated, whereas GRI-977143 inhibited, the invasion of A549-R12 cells. In the presence of LPA, cell viability to cisplatin (CDDP) was higher in A549-R12 cells cultured at both 21 % and 1 % O<sub>2</sub> compared to A549 cells. These results suggest that LPA receptor signaling plays a key role in regulating malignant progression in highly migratory lung cancer cells under hypoxic conditions.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"127 3","pages":"Article 152268"},"PeriodicalIF":2.3,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144123613","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
Non-specific background in immunoglobulin G staining can be effectively eliminated using heating or a catalase inhibitor 免疫球蛋白G染色中的非特异性背景可以通过加热或过氧化氢酶抑制剂有效地消除
IF 2.3 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-05-19 DOI: 10.1016/j.acthis.2025.152269
Kairan Yang , Ting Xu , Chengkang Lin , Zuisu Yang , Haiyan Lyu , Falei Yuan
Immunoglobulin G (IgG) staining is a widely used method for assessing blood-brain barrier (BBB) integrity. However, significant non-specific binding is often observed in many studies, which can interfere with the accurate interpretation of results. In this study, the horseradish peroxidase (HRP)-based polymer method and the streptavidin-biotin complex (SABC) method were used to perform IgG staining. The effects of hydrogen peroxide, heating, and a catalase inhibitor on reducing background staining were evaluated in brain sections from untreated mice and those subjected to middle cerebral artery occlusion (MCAO). The results showed that immunohistochemistry without hydrogen peroxide pretreatment still produced minimal background in paraffin-embedded sections. However, IgG staining with hydrogen peroxide pretreatment led to substantial background in vibratome sections. Compared to the SABC method, a mixture of the catalase inhibitor 3-amino-1,2,4-triazole and hydrogen peroxide reduced background staining by 35.4 % ± 5.7 % in the cortex of untreated mouse brains and by 36.9 % ± 1.8 % in the contralateral cortex of MCAO mice when using the polymer method. Additionally, heating at 75°C was sufficient to eliminate non-specific binding in brain sections from both untreated and MCAO mice. Hydrogen peroxide pretreatment alone was ineffective in removing background staining in brain sections from either untreated or MCAO mice. In summary, this study demonstrates that hydrogen peroxide pretreatment is effective in reducing background only when combined with a catalase inhibitor but is unnecessary when the tissue is heated. Heating is a simple and effective method for removing the IgG staining background when detecting BBB leakage.
免疫球蛋白G (IgG)染色是一种广泛使用的评估血脑屏障(BBB)完整性的方法。然而,在许多研究中经常观察到显著的非特异性结合,这可能会干扰结果的准确解释。本研究采用辣根过氧化物酶(HRP)聚合物法和链亲和素-生物素复合物(SABC)法进行IgG染色。过氧化氢、加热和过氧化氢酶抑制剂对降低背景染色的影响在未治疗的小鼠和大脑中动脉闭塞(MCAO)小鼠的脑切片中进行了评估。结果表明,未经双氧水预处理的免疫组织化学方法在石蜡包埋切片中仍产生极小的背景。然而,过氧化氢预处理的IgG染色在振动体切片中导致大量背景。与SABC方法相比,过氧化氢酶抑制剂3-氨基-1,2,4-三唑和过氧化氢的混合物在使用聚合物方法时,未处理小鼠大脑皮层的背景染色减少35.4% % ± 5.7 %,在MCAO小鼠对侧皮层的背景染色减少36.9 % ± 1.8 %。此外,在75°C下加热足以消除未处理和MCAO小鼠脑切片中的非特异性结合。单独过氧化氢预处理对未处理或MCAO小鼠脑切片的背景染色均无效。总之,这项研究表明,过氧化氢预处理只有在与过氧化氢酶抑制剂联合使用时才能有效地降低背景,而当组织被加热时则没有必要。加热是检测血脑屏障渗漏时去除IgG染色背景的一种简单有效的方法。
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引用次数: 0
Retraction notice to “miR-103–3p attenuates liver injury with severe acute pancreatitis by inhibiting pyroptosis through miR-103-3p/NLRP1 axis” [Acta Histochem. 126 (2024) 152211] 关于“miR-103-3p通过miR-103-3p/NLRP1轴抑制焦亡减轻重症急性胰腺炎肝损伤”的撤回通知[journal of histochemistry . 126(2024) 152211]。
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-05-15 DOI: 10.1016/j.acthis.2025.152258
Wenquan Zhang , Min Du , Yingjian Jiang , Jiang Wang , Yue Yu , DianLiang Zhang
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引用次数: 0
Quantifying mechanical, proliferation, and migrational properties of bulk ovarian cancer cells and ovarian cancer stem cells 定量测定大块卵巢癌细胞和卵巢癌干细胞的力学、增殖和迁移特性
IF 2.3 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-05-10 DOI: 10.1016/j.acthis.2025.152260
Crystal Brown , Emily Stidham , Elly Beck , Ali Eickhoff , Brianna Hill , Kalyani Nair , Craig Cady
There are a limited number of studies analyzing ovarian cancer stem cell properties. The goal of this study was to analyze the mechanical and migrational properties of ovarian cancer stem cells with the well-researched bulk ovarian cancer cells. Through the use of atomic force microscopy (AFM), the mechanical properties of both cell types were gathered. In preparation for AFM analysis, an optimal fixation method was developed and performed on the cells. AFM analysis provided mechanical properties for both cell types, including cellular stiffness, maximum adhesion force, surface area, and mean surface roughness. Cell proliferation and transwell migration assays were assessed to determine the aggressiveness of both cancer cell types. A clear trend between both cell types was expected for the mechanical and potential aggression properties. The data from both analyses were used to create a baseline for migration, proliferation, and mechanical properties of ovarian cancer stem cells and bulk ovarian cancer cells. Further studies will assess if these properties are impacted by chemotherapy exposure.
分析卵巢癌干细胞特性的研究数量有限。本研究的目的是分析卵巢癌干细胞的力学和迁移特性与大量研究的卵巢癌细胞。通过原子力显微镜(AFM),收集了两种细胞类型的力学性能。为了准备AFM分析,我们开发了一种最佳的固定方法并对细胞进行了固定。AFM分析提供了两种细胞类型的力学性能,包括细胞刚度、最大附着力、表面积和平均表面粗糙度。评估细胞增殖和跨井迁移试验以确定两种癌细胞类型的侵袭性。两种细胞类型在机械和潜在的攻击特性上有明显的趋势。这两项分析的数据被用来创建卵巢癌干细胞和散装卵巢癌细胞的迁移、增殖和力学特性的基线。进一步的研究将评估这些特性是否受到化疗暴露的影响。
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引用次数: 0
期刊
Acta histochemica
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