Pub Date : 2024-12-01Epub Date: 2024-09-16DOI: 10.1016/j.acthis.2024.152194
J.J. Rodríguez , E. Gardenal , F. Zallo , J. Cabot , X. Busquets
Neurodegenerative diseases such as Alzheimer´s (AD) and physiological ageing are characterized by a decline in neurogenesis and in the polysialylated isoforms of neural cell adhesion molecule (PSA-NCAM) expression within the hippocampus and specifically in the dentate gyrus (DG). In the 3xTG-AD mouse model, which mimics the human disease in both pathological and behavioral features, this decline in PSA-NCAM is associated with the presence of Aβ plaques at 9 months and Tau tangles at 12–15 months. In this work we studied the presence of PSA-NCAM at early ages (1–6 months) in the same model. Our results demonstrated that even as early as the first month of age there is a strong decrease in PSA-NCAM dendritic tree mainly altering the molecular layer (MolL) coverage affecting the synaptic plasticity and furthermore confirmed by the reduction of PSA-NCAM area density (Sv) in the 3xTG-AD. Similar and more marked early changes were seen during aging in both NTG and 3xTg-AD animals. Our results demonstrate for the first time a precipitate decrease of PSA-NCAM cells at such very early phases of the disease. This result suggests an early effect of the disease in the progression of immature and pluripotent cells resulting in an ulterior and early diminution of neurogenesis and therefore an impaired hippocampal cellular and synaptic plasticity.
{"title":"Early PSA-NCAM reduction in the dentate gyrus and impaired plasticity in the Alzheimer´s disease 3xTg-mice model","authors":"J.J. Rodríguez , E. Gardenal , F. Zallo , J. Cabot , X. Busquets","doi":"10.1016/j.acthis.2024.152194","DOIUrl":"10.1016/j.acthis.2024.152194","url":null,"abstract":"<div><p>Neurodegenerative diseases such as Alzheimer´s (AD) and physiological ageing are characterized by a decline in neurogenesis and in the polysialylated isoforms of neural cell adhesion molecule (PSA-NCAM) expression within the hippocampus and specifically in the dentate gyrus (DG). In the 3xTG-AD mouse model, which mimics the human disease in both pathological and behavioral features, this decline in PSA-NCAM is associated with the presence of Aβ plaques at 9 months and Tau tangles at 12–15 months. In this work we studied the presence of PSA-NCAM at early ages (1–6 months) in the same model. Our results demonstrated that even as early as the first month of age there is a strong decrease in PSA-NCAM dendritic tree mainly altering the molecular layer (MolL) coverage affecting the synaptic plasticity and furthermore confirmed by the reduction of PSA-NCAM area density (Sv) in the 3xTG-AD. Similar and more marked early changes were seen during aging in both NTG and 3xTg-AD animals. Our results demonstrate for the first time a precipitate decrease of PSA-NCAM cells at such very early phases of the disease. This result suggests an early effect of the disease in the progression of immature and pluripotent cells resulting in an ulterior and early diminution of neurogenesis and therefore an impaired hippocampal cellular and synaptic plasticity.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"126 8","pages":"Article 152194"},"PeriodicalIF":2.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142243148","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}
Pub Date : 2024-12-01Epub Date: 2024-10-16DOI: 10.1016/j.acthis.2024.152204
Momoka Shobudani , Yuri Sakamaki , Ayumi Karasawa , Ryota Ojiro , Xinyu Zou , Qian Tang , Shunsuke Ozawa , Meilan Jin , Toshinori Yoshida , Makoto Shibutani
Fluoride affects neurodevelopment in children. In this study, we examined the effects of developmental exposure to sodium fluoride (NaF) on hippocampal neurogenesis in rats. Dams were given drinking water containing NaF at 0 (untreated controls), 30 or 100 ppm from gestational day 6 to day 21 post-delivery upon weaning, and offspring were reared until postnatal day (PND) 77. On PND 21, NaF at 100 ppm altered the numbers in subpopulations of granule cell lineages, including a decrease in type-3 neural progenitor cells (NPCs), as well as a compensatory increase in type-1 neural stem cells (NSCs) and type-2a NPCs. NaF exposure tended to increase GluR2+ mossy cells in the hilus of the dentate gyrus (DG) in a dose-dependent manner, suggesting that NaF exposure induces a compensatory neurogenic response. NaF also caused a dose-dependent increase in ARC+ granule cells, and it upregulated Ptgs2 in the DG at 100 ppm, suggesting that NaF exposure increases synaptic plasticity in granule cells. NaF at 100 ppm upregulated granule cell lineage marker genes (Nes, Eomes and Rbfox3) and an anti-apoptotic gene (Bcl2), suggesting ameliorating responses against the impaired neurogenesis during NaF exposure. Moreover, NaF at 100 ppm downregulated oxidative phosphorylation-related genes (Atp5f1b and Sdhd) and upregulated a glycolysis-related gene (Hk3), suggesting a metabolic shift in cells undergoing neurogenesis. By PND 77, the changes in granule cell lineages were no longer detected, and GABAergic interneuron marker genes (Calb2 and Reln) were upregulated, suggesting a persistent protective response in granule cell lineages. Together, these findings suggest that developmental NaF exposure causes transient disruption of hippocampal neurogenesis, which in turn induces a metabolic shift as a compensatory response.
{"title":"Metabolic shift as a compensatory response to impaired hippocampal neurogenesis after developmental exposure to sodium fluoride in rats","authors":"Momoka Shobudani , Yuri Sakamaki , Ayumi Karasawa , Ryota Ojiro , Xinyu Zou , Qian Tang , Shunsuke Ozawa , Meilan Jin , Toshinori Yoshida , Makoto Shibutani","doi":"10.1016/j.acthis.2024.152204","DOIUrl":"10.1016/j.acthis.2024.152204","url":null,"abstract":"<div><div>Fluoride affects neurodevelopment in children. In this study, we examined the effects of developmental exposure to sodium fluoride (NaF) on hippocampal neurogenesis in rats. Dams were given drinking water containing NaF at 0 (untreated controls), 30 or 100 ppm from gestational day 6 to day 21 post-delivery upon weaning, and offspring were reared until postnatal day (PND) 77. On PND 21, NaF at 100 ppm altered the numbers in subpopulations of granule cell lineages, including a decrease in type-3 neural progenitor cells (NPCs), as well as a compensatory increase in type-1 neural stem cells (NSCs) and type-2a NPCs. NaF exposure tended to increase GluR2<sup>+</sup> mossy cells in the hilus of the dentate gyrus (DG) in a dose-dependent manner, suggesting that NaF exposure induces a compensatory neurogenic response. NaF also caused a dose-dependent increase in ARC<sup>+</sup> granule cells, and it upregulated <em>Ptgs2</em> in the DG at 100 ppm, suggesting that NaF exposure increases synaptic plasticity in granule cells. NaF at 100 ppm upregulated granule cell lineage marker genes (<em>Nes</em>, <em>Eomes</em> and <em>Rbfox3</em>) and an anti-apoptotic gene (<em>Bcl2</em>), suggesting ameliorating responses against the impaired neurogenesis during NaF exposure. Moreover, NaF at 100 ppm downregulated oxidative phosphorylation-related genes (<em>Atp5f1b</em> and <em>Sdhd</em>) and upregulated a glycolysis-related gene (<em>Hk3</em>), suggesting a metabolic shift in cells undergoing neurogenesis. By PND 77, the changes in granule cell lineages were no longer detected, and GABAergic interneuron marker genes (<em>Calb2</em> and <em>Reln</em>) were upregulated, suggesting a persistent protective response in granule cell lineages. Together, these findings suggest that developmental NaF exposure causes transient disruption of hippocampal neurogenesis, which in turn induces a metabolic shift as a compensatory response.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"126 8","pages":"Article 152204"},"PeriodicalIF":2.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142441519","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}
Pub Date : 2024-12-01Epub Date: 2024-10-30DOI: 10.1016/j.acthis.2024.152211
Wenquan Zhang , Min Du , Yingjian Jiang , Jiang Wang , Yue Yu , DianLiang Zhang
Background
Severe acute pancreatitis (SAP) is a common digestive system disorder in clinical practice, and it is often associated with liver damage in patients with severe acute pancreatitis. Several studies have indicated that pyroptosis plays a role in liver damage following severe acute pancreatitis (SAP). However, the precise mechanisms remain unclear. This study aims to elucidate the association and specific mechanisms between liver injury following SAP and pyroptosis, providing theoretical support for research on SAP-induced liver injury.
Methods
A rat model of SAP with concomitant liver injury was successfully established. The expression levels of miR-103–3p across different liver tissue groups were quantified using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). Bioinformatic analyses and dual-luciferase reporter assays confirmed that NLRP1 is a direct target of miR-103–3p. In vivo assessments of miR-103–3p levels were performed, and the extent of cell pyroptosis during liver injury post-SAP was evaluated through western blotting, qRT-PCR, scanning electron microscopy, histopathology, immunofluorescence, and immunohistochemistry. The role of miR-103–3p in regulating NLRP1-mediated pyroptosis and its impact on SAP-induced liver injury were validated.
Results
This study reports that following SAP-induced liver injury, the expression of miR-103–3p in liver tissue was significantly decreased, and cell pyroptosis was involved in the process of liver injury. Experimental validation indicated that NLRP1 was a downstream target of miR-103–3p. Overexpression of miR-103–3p in vitro significantly alleviated the severity of liver injury following SAP, while simultaneously inhibiting cell pyroptosis.
Conclusion
These findings indicate that pyroptosis may be linked to SAP-induced liver injury and that miR-103–3p mitigates hepatocyte pyroptosis by reducing liver injury through the suppression of NLRP1 expression.
背景：重症急性胰腺炎（SAP）是临床上常见的消化系统疾病，重症急性胰腺炎患者往往伴有肝损伤。一些研究表明，热蛋白沉积在重症急性胰腺炎（SAP）后的肝损伤中起一定作用。然而，其确切机制仍不清楚。本研究旨在阐明 SAP 后肝损伤与热蛋白沉积之间的关联和具体机制，为 SAP 诱导肝损伤的研究提供理论支持：方法：成功建立了伴有肝损伤的 SAP 大鼠模型。方法：成功建立了伴有肝损伤的 SAP 大鼠模型，并利用定量反转录聚合酶链反应（qRT-PCR）对不同肝组织组 miR-103-3p 的表达水平进行了定量分析。生物信息学分析和双荧光素酶报告实验证实，NLRP1 是 miR-103-3p 的直接靶标。研究人员对 miR-103-3p 的水平进行了体内评估，并通过 Western 印迹、qRT-PCR、扫描电子显微镜、组织病理学、免疫荧光和免疫组织化学等方法评估了 SAP 后肝损伤过程中细胞热解的程度。研究验证了 miR-103-3p 在调控 NLRP1 介导的热蛋白沉积中的作用及其对 SAP 诱导的肝损伤的影响：结果：本研究发现，SAP 诱导的肝损伤后，肝组织中 miR-103-3p 的表达明显降低，细胞裂解参与了肝损伤的过程。实验验证表明，NLRP1是miR-103-3p的下游靶标。在体外过表达 miR-103-3p 能明显减轻 SAP 损伤后肝损伤的严重程度，同时抑制细胞嗜热：这些研究结果表明，肝细胞脓毒症可能与 SAP 诱导的肝损伤有关，而 miR-103-3p 可通过抑制 NLRP1 的表达减轻肝损伤，从而缓解肝细胞脓毒症。
{"title":"miR-103–3p attenuates liver injury with severe acute pancreatitis by inhibiting pyroptosis through miR-103–3p/NLRP1 axis","authors":"Wenquan Zhang , Min Du , Yingjian Jiang , Jiang Wang , Yue Yu , DianLiang Zhang","doi":"10.1016/j.acthis.2024.152211","DOIUrl":"10.1016/j.acthis.2024.152211","url":null,"abstract":"<div><h3>Background</h3><div>Severe acute pancreatitis (SAP) is a common digestive system disorder in clinical practice, and it is often associated with liver damage in patients with severe acute pancreatitis. Several studies have indicated that pyroptosis plays a role in liver damage following severe acute pancreatitis (SAP). However, the precise mechanisms remain unclear. This study aims to elucidate the association and specific mechanisms between liver injury following SAP and pyroptosis, providing theoretical support for research on SAP-induced liver injury.</div></div><div><h3>Methods</h3><div>A rat model of SAP with concomitant liver injury was successfully established. The expression levels of miR-103–3p across different liver tissue groups were quantified using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). Bioinformatic analyses and dual-luciferase reporter assays confirmed that NLRP1 is a direct target of miR-103–3p. In vivo assessments of miR-103–3p levels were performed, and the extent of cell pyroptosis during liver injury post-SAP was evaluated through western blotting, qRT-PCR, scanning electron microscopy, histopathology, immunofluorescence, and immunohistochemistry. The role of miR-103–3p in regulating NLRP1-mediated pyroptosis and its impact on SAP-induced liver injury were validated.</div></div><div><h3>Results</h3><div>This study reports that following SAP-induced liver injury, the expression of miR-103–3p in liver tissue was significantly decreased, and cell pyroptosis was involved in the process of liver injury. Experimental validation indicated that NLRP1 was a downstream target of miR-103–3p. Overexpression of miR-103–3p in vitro significantly alleviated the severity of liver injury following SAP, while simultaneously inhibiting cell pyroptosis.</div></div><div><h3>Conclusion</h3><div>These findings indicate that pyroptosis may be linked to SAP-induced liver injury and that miR-103–3p mitigates hepatocyte pyroptosis by reducing liver injury through the suppression of NLRP1 expression.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"126 8","pages":"Article 152211"},"PeriodicalIF":2.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142542953","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}
Pub Date : 2024-12-01Epub Date: 2024-09-06DOI: 10.1016/j.acthis.2024.152188
Ting Sun , Liming Xu , Hongtian Yao , Jing Zhao , Zhen Chen , Zexin Chen , Bo Wang , Wei Ding
Bone marrow biopsy depends on tissue morphology, immunohistochemical staining, and moleculardetection. Tissue pretreatment is required for bone marrow samples, from clinical specimen acquisition to pathological reporting, but during the process, proteins and nucleic acids are often altered because of the acid in fixation and decalcification solutions. In our study, we present an easy and effective pretreatment protocol and compared this novel pretreatment protocol (Set 2) with an existing traditional pretreatment process (Set 1) using tissue morphology, IHC staining, and molecular pathological analyses. Granulocytic IHC markers showed more intensive staining in samples of Set 2 than in those of Set 1. The Set 2 protocol provided a higher DNA yield and less fragmentation; moreover, samples processed with the Set 2 protocol could be subsequently used in FISH and DNA sequencing assays. Our optimized novel pretreatment protocol could better protect proteins and DNA molecules while maintaining good cell morphology compared to traditional pretreatment The novel pretreatment reagents could role as a reference by more laboratories for pretreating bone marrow biopsy samples and scientific research.
骨髓活检取决于组织形态、免疫组化染色和分子检测。从临床标本采集到病理报告，骨髓样本都需要进行组织预处理，但在这一过程中，蛋白质和核酸往往会因固定和脱钙溶液中的酸而发生改变。在我们的研究中，我们提出了一种简便有效的预处理方案，并利用组织形态学、IHC 染色和分子病理学分析比较了这种新型预处理方案（Set 2）和现有的传统预处理流程（Set 1）。与第一套方案相比，第二套方案样本中的粒细胞 IHC 标记显示出更密集的染色。第2套方案的DNA产量更高，碎片更少；此外，用第2套方案处理的样本随后还可用于FISH和DNA测序检测。与传统预处理相比，我们优化的新型预处理方案能更好地保护蛋白质和 DNA 分子，同时保持良好的细胞形态。新型预处理试剂可为更多实验室对骨髓活检样本进行预处理和科学研究提供参考。
{"title":"A set of pretreatment reagents including improved formula fixation and decalcification facilitating immunohistochemistry and DNA analyses of formalin-fixed paraffin-embedded bone marrow trephine biopsy","authors":"Ting Sun , Liming Xu , Hongtian Yao , Jing Zhao , Zhen Chen , Zexin Chen , Bo Wang , Wei Ding","doi":"10.1016/j.acthis.2024.152188","DOIUrl":"10.1016/j.acthis.2024.152188","url":null,"abstract":"<div><p>Bone marrow biopsy depends on tissue morphology, immunohistochemical staining, and moleculardetection. Tissue pretreatment is required for bone marrow samples, from clinical specimen acquisition to pathological reporting, but during the process, proteins and nucleic acids are often altered because of the acid in fixation and decalcification solutions. In our study, we present an easy and effective pretreatment protocol and compared this novel pretreatment protocol (Set 2) with an existing traditional pretreatment process (Set 1) using tissue morphology, IHC staining, and molecular pathological analyses. Granulocytic IHC markers showed more intensive staining in samples of Set 2 than in those of Set 1. The Set 2 protocol provided a higher DNA yield and less fragmentation; moreover, samples processed with the Set 2 protocol could be subsequently used in FISH and DNA sequencing assays. Our optimized novel pretreatment protocol could better protect proteins and DNA molecules while maintaining good cell morphology compared to traditional pretreatment The novel pretreatment reagents could role as a reference by more laboratories for pretreating bone marrow biopsy samples and scientific research.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"126 8","pages":"Article 152188"},"PeriodicalIF":2.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142144911","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}
The carotid body is a hypoxia-sensitive chemoreceptor that induces sensory long-term facilitation after exposure to chronic intermittent hypoxia. However, the mechanisms underlying synaptic plasticity in the carotid body remain unknown. In the present study, we examined the immunohistochemical distribution of cannabinoid receptor type 1 (CB1) and type 2 (CB2), which are candidate molecules involved in the modulation of synaptic transmission. Dot-like CB1 immunoreactivity was distributed in the perinuclear cytoplasm of chemoreceptor cells immunoreactive for the catecholamine-synthesizing enzymes, tyrosine hydroxylase and dopamine beta-hydroxylase. Furthermore, CB1 immunoreactivity was observed in sensory nerve endings immunoreactive for P2X3 purinoceptors that colocalized with vesicular glutamate transporter 2. On the other hand, immunoreactivity for CB2 was mainly distributed in chemoreceptor cells, and was weakly observed in sensory nerve endings immunoreactive for P2X2 purinoceptors. The present results suggest that CB1 and CB2 regulate the release of catecholamines and glutamate from chemoreceptor cells and sensory nerve endings, respectively. Therefore, CB1 and CB2 may be involved in synaptic plasticity in the carotid body.
{"title":"Immunohistochemical distribution of cannabinoid receptor type 1 (CB1) and type 2 (CB2) in the rat carotid body","authors":"Hiroki Saito, Takuya Yokoyama , Nobuaki Nakamuta, Yoshio Yamamoto","doi":"10.1016/j.acthis.2024.152205","DOIUrl":"10.1016/j.acthis.2024.152205","url":null,"abstract":"<div><div>The carotid body is a hypoxia-sensitive chemoreceptor that induces sensory long-term facilitation after exposure to chronic intermittent hypoxia. However, the mechanisms underlying synaptic plasticity in the carotid body remain unknown. In the present study, we examined the immunohistochemical distribution of cannabinoid receptor type 1 (CB1) and type 2 (CB2), which are candidate molecules involved in the modulation of synaptic transmission. Dot-like CB1 immunoreactivity was distributed in the perinuclear cytoplasm of chemoreceptor cells immunoreactive for the catecholamine-synthesizing enzymes, tyrosine hydroxylase and dopamine beta-hydroxylase. Furthermore, CB1 immunoreactivity was observed in sensory nerve endings immunoreactive for P2X<sub>3</sub> purinoceptors that colocalized with vesicular glutamate transporter 2. On the other hand, immunoreactivity for CB2 was mainly distributed in chemoreceptor cells, and was weakly observed in sensory nerve endings immunoreactive for P2X<sub>2</sub> purinoceptors. The present results suggest that CB1 and CB2 regulate the release of catecholamines and glutamate from chemoreceptor cells and sensory nerve endings, respectively. Therefore, CB1 and CB2 may be involved in synaptic plasticity in the carotid body.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"126 8","pages":"Article 152205"},"PeriodicalIF":2.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142434521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01Epub Date: 2024-09-28DOI: 10.1016/j.acthis.2024.152192
Mengran Wang , Tingting Xuan , Haining Li , Jing An , Tianhui He , Jiang Cheng
{"title":"Corrigendum to “Protective effect of FXN overexpression on ferroptosis in L-Glu-induced SH-SY5Y cells” [Acta Histochem. 126 (2024) 152135]","authors":"Mengran Wang , Tingting Xuan , Haining Li , Jing An , Tianhui He , Jiang Cheng","doi":"10.1016/j.acthis.2024.152192","DOIUrl":"10.1016/j.acthis.2024.152192","url":null,"abstract":"","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"126 8","pages":"Article 152192"},"PeriodicalIF":2.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339039","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}
Neuronal splicing regulator RNA binding protein, fox-1 homolog 3 (NeuN/RbFox3), is expressed in postmitotic neurons and distributed heterogeneously in the cell. During excitotoxicity events caused by the excess glutamate, several alterations that culminate in neuronal death have been described. However, NeuN/RbFox3 organization and distribution are still unknown. Therefore, our objective was to analyze the nucleocytoplasmic distribution and organization of NeuN/RbFox3 in hippocampal and cortical neurons using an excitotoxicity model with monosodium glutamate salt (MSG). We used neonatal Wistar rats administered subcutaneously with 4 MSG mg/kg during the postnatal day (PND) 1, 3, 5, and 7. The control group was rats without MSG administration. On 14 PND, the brain was removed, and coronal sections were used for immunodetection with the antibody NeuN, DAPI, and the propidium iodide staining for histological evaluation. The results indicate that in the control group, NeuN/RbFox3 was organized into macromolecular condensates inside and outside the nucleus, forming defined nuclear compartments. Additionally, NeuN/RbFox3 was distributed proximal to the nucleus in the cytoplasm. In contrast, in the group treated with MSG, the distribution was diffuse and dispersed in the nucleus and cytoplasm without the formation of compartments in the nucleus. Our findings, which highlight the significant impact of MSG administration in the neonatal period on the distribution and organization of NeuN/RbFox3 of neurons in the hippocampus and cerebral cortex, offer a new perspective to investigate MSG alterations in the developmental brain.
{"title":"Neuronal splicing regulator RBFOX3 (NeuN) distribution and organization are modified in response to monosodium glutamate in rat brain at postnatal day 14","authors":"Anaís Monzerrat García Juárez, Nidia Jannette Carrillo González, Tania Campos-Ordoñez, Yadira Gasca Martínez, Graciela Gudiño-Cabrera","doi":"10.1016/j.acthis.2024.152207","DOIUrl":"10.1016/j.acthis.2024.152207","url":null,"abstract":"<div><div>Neuronal splicing regulator RNA binding protein, fox-1 homolog 3 (NeuN/RbFox3), is expressed in postmitotic neurons and distributed heterogeneously in the cell. During excitotoxicity events caused by the excess glutamate, several alterations that culminate in neuronal death have been described. However, NeuN/RbFox3 organization and distribution are still unknown. Therefore, our objective was to analyze the nucleocytoplasmic distribution and organization of NeuN/RbFox3 in hippocampal and cortical neurons using an excitotoxicity model with monosodium glutamate salt (MSG). We used neonatal Wistar rats administered subcutaneously with 4 MSG mg/kg during the postnatal day (PND) 1, 3, 5, and 7. The control group was rats without MSG administration. On 14 PND, the brain was removed, and coronal sections were used for immunodetection with the antibody NeuN, DAPI, and the propidium iodide staining for histological evaluation. The results indicate that in the control group, NeuN/RbFox3 was organized into macromolecular condensates inside and outside the nucleus, forming defined nuclear compartments. Additionally, NeuN/RbFox3 was distributed proximal to the nucleus in the cytoplasm. In contrast, in the group treated with MSG, the distribution was diffuse and dispersed in the nucleus and cytoplasm without the formation of compartments in the nucleus. Our findings, which highlight the significant impact of MSG administration in the neonatal period on the distribution and organization of NeuN/RbFox3 of neurons in the hippocampus and cerebral cortex, offer a new perspective to investigate MSG alterations in the developmental brain.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"126 8","pages":"Article 152207"},"PeriodicalIF":2.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142455444","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}
Pub Date : 2024-12-01Epub Date: 2024-10-30DOI: 10.1016/j.acthis.2024.152213
Lorenzo Alibardi
An electron microscopy and immunohistochemistry study has been conducted to acquire comparative information on the structure of apteric skin in ratites, ostrich and emu. The epidermis is thin in the neck of both species and thicker in the dorsal region where acidic and neutral keratins are present in the viable epidermis and stratum corneum. The dermis in both species is mostly occupied by collagen fibrils that form large bundles, often organized in alternated layers in the deeper part of the dermis. Numerous collagen fibrils contact the basement membrane of the epidermis. Sparse tactile Meissner or Krause sensilli are present among the thick collagen bundles. The ostrich epidermis in the dorsal skin is thicker than in the neck, with a columnar basal layer, 3–5 intermediate suprabasal layers and a thick corneous layer. The epidermis of the neck in emu is very thin, featuring two-three narrow cell layers above a flat basal layer and a relatively thick corneous layer. Basal and suprabasal keratinocytes contain lipid droplets and small keratin bundles but no keratohyalin accumulates in pre-corneous cells. The thin corneocytes form a multilayered corneous layer. Loricrine is present in pre-corneous and corneous layers while CBPs, formerly indicated as beta-keratins, are absent in apteric epidermis.
{"title":"Ultrastructure and immunohistochemistry of apteric skin in ratites and its epidermal soft cornification","authors":"Lorenzo Alibardi","doi":"10.1016/j.acthis.2024.152213","DOIUrl":"10.1016/j.acthis.2024.152213","url":null,"abstract":"<div><div>An electron microscopy and immunohistochemistry study has been conducted to acquire comparative information on the structure of apteric skin in ratites, ostrich and emu. The epidermis is thin in the neck of both species and thicker in the dorsal region where acidic and neutral keratins are present in the viable epidermis and stratum corneum. The dermis in both species is mostly occupied by collagen fibrils that form large bundles, often organized in alternated layers in the deeper part of the dermis. Numerous collagen fibrils contact the basement membrane of the epidermis. Sparse tactile Meissner or Krause sensilli are present among the thick collagen bundles. The ostrich epidermis in the dorsal skin is thicker than in the neck, with a columnar basal layer, 3–5 intermediate suprabasal layers and a thick corneous layer. The epidermis of the neck in emu is very thin, featuring two-three narrow cell layers above a flat basal layer and a relatively thick corneous layer. Basal and suprabasal keratinocytes contain lipid droplets and small keratin bundles but no keratohyalin accumulates in pre-corneous cells. The thin corneocytes form a multilayered corneous layer. Loricrine is present in pre-corneous and corneous layers while CBPs, formerly indicated as beta-keratins, are absent in apteric epidermis.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"126 8","pages":"Article 152213"},"PeriodicalIF":2.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142542954","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}
Pub Date : 2024-12-01Epub Date: 2024-10-31DOI: 10.1016/j.acthis.2024.152212
Lei Yan , Guangyue Luo , Chengxiang Han , Jialin Meng , Chaozhao Liang
This study investigates the role of autophagy-related genes (ARGs) in bladder cancer (BLCA), focusing on the regulator of G protein signaling 19 (RGS19). Using data from The Cancer Genome Atlas (TCGA) and the Human Autophagy Database (HADb), we identified RGS19 as significantly upregulated and linked to poor prognosis in BLCA. Kaplan-Meier survival analysis confirmed its association with increased mortality and. In vitro, RGS19 knockdown in BLCA cell lines inhibited proliferation, migration, and invasion, while inducing apoptosis and autophagy. Transmission electron microscopy showed autophagic structures in RGS19-silenced cells. In vivo, a xenograft mouse model demonstrated reduced tumor growth with RGS19 knockdown. Immunohistochemical (IHC) analysis revealed decreased Ki67 and increased autophagy markers in tumors with reduced RGS19. Pathway analysis suggested RGS19 acts through the cGMP-PKG signaling pathway, validated by altered expression of soluble guanylate cyclase (sGC), protein kinase G (PKG1), phosphodiesterase 5 A (PDE5A), vasodilator-stimulated phosphoprotein (VASP), and phosphorylated VASP (p-VASP) upon RGS19 knockdown. These results highlight RGS19 as a potential biomarker and therapeutic target in BLCA.
{"title":"Exploring the oncogenic role of RGS19 in bladder cancer progression and prognosis","authors":"Lei Yan , Guangyue Luo , Chengxiang Han , Jialin Meng , Chaozhao Liang","doi":"10.1016/j.acthis.2024.152212","DOIUrl":"10.1016/j.acthis.2024.152212","url":null,"abstract":"<div><div>This study investigates the role of autophagy-related genes (ARGs) in bladder cancer (BLCA), focusing on the regulator of G protein signaling 19 (RGS19). Using data from The Cancer Genome Atlas (TCGA) and the Human Autophagy Database (HADb), we identified RGS19 as significantly upregulated and linked to poor prognosis in BLCA. Kaplan-Meier survival analysis confirmed its association with increased mortality and. In vitro, RGS19 knockdown in BLCA cell lines inhibited proliferation, migration, and invasion, while inducing apoptosis and autophagy. Transmission electron microscopy showed autophagic structures in RGS19-silenced cells. In vivo, a xenograft mouse model demonstrated reduced tumor growth with RGS19 knockdown. Immunohistochemical (IHC) analysis revealed decreased Ki67 and increased autophagy markers in tumors with reduced RGS19. Pathway analysis suggested RGS19 acts through the cGMP-PKG signaling pathway, validated by altered expression of soluble guanylate cyclase (sGC), protein kinase G (PKG1), phosphodiesterase 5 A (PDE5A), vasodilator-stimulated phosphoprotein (VASP), and phosphorylated VASP (p-VASP) upon RGS19 knockdown. These results highlight RGS19 as a potential biomarker and therapeutic target in BLCA.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"126 8","pages":"Article 152212"},"PeriodicalIF":2.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142553255","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}
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