Acta histochemica最新文献

{"title":"Classification of colorectal cancer consensus molecular subtypes using attention-based multi-instance learning network on whole-slide images","authors":"Huilin Xu ,&nbsp;Aoshen Wu ,&nbsp;He Ren ,&nbsp;Chenghang Yu ,&nbsp;Gang Liu ,&nbsp;Lei Liu","doi":"10.1016/j.acthis.2023.152057","DOIUrl":"10.1016/j.acthis.2023.152057","url":null,"abstract":"<div><p>Colorectal cancer (CRC) is the third most common and second most lethal cancer globally. It is highly heterogeneous with different clinical-pathological characteristics, prognostic status, and therapy responses. Thus, the precise diagnosis of CRC subtypes is of great significance for improving the prognosis and survival of CRC patients. Nowadays, the most commonly used molecular-level CRC classification system is the Consensus Molecular Subtypes (CMSs). In this study, we applied a weakly supervised deep learning method, named attention-based multi-instance learning (MIL), on formalin-fixed paraffin-embedded (FFPE) whole-slide images (WSIs) to distinguish CMS1 subtype from CMS2, CMS3, and CMS4 subtypes, as well as distinguish CMS4 from CMS1, CMS2, and CMS3 subtypes. The advantage of MIL is training a bag of the tiled instance with bag-level labels only. Our experiment was performed on 1218 WSIs obtained from The Cancer Genome Atlas (TCGA). We constructed three convolutional neural network-based structures for model training and evaluated the ability of the max-pooling operator and mean-pooling operator on aggregating bag-level scores. The results showed that the 3-layer model achieved the best performance in both comparison groups. When compared CMS1 with CMS234, max-pooling reached the ACC of 83.86 % and the mean-pooling operator reached the AUC of 0.731. While comparing CMS4 with CMS123, mean-pooling reached the ACC of 74.26 % and max-pooling reached the AUC of 0.609. Our results implied that WSIs could be utilized to classify CMSs, and manual pixel-level annotation is not a necessity for computational pathology imaging analysis.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10010939","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}

{"title":"Corrigendum to “Hypoxia activates the PI3K/AKT/HIF-1α pathway to promote the anti-inflammatory effect of adipose mesenchymal stem cells” [Acta Histochem.125(4) (2023) 152042]","authors":"Hongjing Ren ,&nbsp;Mengchang Liu ,&nbsp;Yueda Jihu ,&nbsp;Huizhen Zeng ,&nbsp;Chong Yao ,&nbsp;Hong Yan","doi":"10.1016/j.acthis.2023.152076","DOIUrl":"10.1016/j.acthis.2023.152076","url":null,"abstract":"","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10004264","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}

{"title":"Phospholysine phosphohistidine inorganic pyrophosphate phosphatase suppresses human esophageal cancer cell growth by inducing mitotic catastrophe through the P27/cyclin A/CDK2 signaling pathway","authors":"Duan Ruifang ,&nbsp;Yang Changqing ,&nbsp;Ren Chenxia ,&nbsp;Li Ji ,&nbsp;Wei Zibai","doi":"10.1016/j.acthis.2023.152066","DOIUrl":"10.1016/j.acthis.2023.152066","url":null,"abstract":"<div><p><span>Esophageal cancer (ESCA) is a global dead malignancy with poor prognosis. However, its underlying molecular mechanism remains to be elucidated. Phospholysine phosphohistidine </span>inorganic pyrophosphate<span><span><span><span> phosphatase (LHPP) has been reported as a </span>tumor suppressor in multisystem cancer but its function in ESCA has not been reported. We analyzed LHPP expression between normal and tumor tissues of ESCA patients and performed LHPP overexpression on the </span>ESCA cells<span><span> KYSE-150 (K150). We did not observe significant differences in the expression level of LHPP between ESCA and normal tissue, and noticed that LHPP expression was not related to ESCA patient survival rate. However, increased expression of LHPP in K150 cells induced mitochondrial dysfunction, inhibited cell proliferation, migration, and cell cycle, and simultaneously increased cell </span>apoptosis. Besides, we found that K150 cells underwent </span></span>mitotic catastrophe<span> after overexpressing LHPP, which may be regulated through the P27/cyclin A/cdk2 signaling pathway. Although the expression of LHPP may not be related to the progression and prognosis of ESCA, mitotic catastrophe, a new mechanism of tumor suppressor function of LHPP was found after overexpressing LHPP in ESCA cells.</span></span></p></div><div><h3>Data Availability</h3><p>The data used to support the findings of this study are included within the article.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10314519","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}

{"title":"MCM5 is an oncogene of colon adenocarcinoma and promotes progression through cell cycle control","authors":"Jiayan Mao ,&nbsp;Jian Shen ,&nbsp;Xuemei Lu ,&nbsp;Ying Cai ,&nbsp;Rujia Tao ,&nbsp;Yuqin Deng ,&nbsp;Yuanting Zhang ,&nbsp;Yuan Wu ,&nbsp;Wei Chen","doi":"10.1016/j.acthis.2023.152072","DOIUrl":"10.1016/j.acthis.2023.152072","url":null,"abstract":"<div><p>Many patients with colon adenocarcinoma (COAD) are diagnosed at an advanced stage, and the molecular mechanism of COAD progression is intricate and controversial. Therefore, there is an urgent need to identify more novel prognosis biomarkers for COAD and elucidate the molecular mechanism of this disease. The present study aimed to screen out key genes correlated with COAD prognosis. In this study, a key module was identified and four hub genes (MCM5 (encoding minichromosome maintenance complex component 5), NOLC1 (encoding nucleolar and coiled-body phosphoprotein 1), MYC (encoding MYC proto-oncogene, BHLH transcription factor), and CDK4 (encoding cyclin dependent kinase 4)) were selected that correlated with COAD prognosis, based on the GSE9348 dataset in Gene Expression Omnibus database. Gene ontology enrichment and Kyoto Encyclopedia of Genes and Genomes pathway analysis indicated that MCM5 correlated with the cell cycle. Furthermore, MCM5 expression was upregulated in tumor tissues of patients with COAD compared with that in adjacent tissues, based on various databases, including The Cancer Genome Atlas, the Clinical Proteomic Tumor Analysis Consortium database, and the Human Protein Atlas database. Small interfering RNA-mediated knockdown of MCM5 inhibited the cell cycle and migration of colorectal cancer cells in vitro. And western blotting results indicated that factors correlated with cell cycle (CDK2/6, Cyclin D3, P21) were downregulated after knockdown of MCM5 in vitro. Besides, downregulation of MCM5 was demonstrated to inhibit lung metastasis of COAD in nude mice model. In conclusion, MCM5 is an oncogene of COAD that promotes COAD progression via cell cycle control.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9963860","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}

{"title":"Resveratrol as an antitumor agent for glioblastoma multiforme: Targeting resistance and promoting apoptotic cell deaths","authors":"Sepideh Karkon-Shayan ,&nbsp;Hasan Aliashrafzadeh ,&nbsp;Hassan Dianat-Moghadam ,&nbsp;Nima Rastegar-Pouyani ,&nbsp;Mohammadreza Majidi ,&nbsp;Mahdi Zarei ,&nbsp;Sadegh moradi-vastegani ,&nbsp;Yaser Bahramvand ,&nbsp;Sepideh Babaniamansour ,&nbsp;Emad Jafarzadeh","doi":"10.1016/j.acthis.2023.152058","DOIUrl":"10.1016/j.acthis.2023.152058","url":null,"abstract":"<div><p>Glioblastoma multiforme<span><span> (GBM) is one of the most aggressive brain and spinal cord tumors<span>. Despite the significant development in application of antitumor drugs, no significant increases have been observed in the survival rates of patients with GBM, as GBM cells acquire resistance to conventional anticancer therapeutic agents. Multiple studies have revealed that PI3K/Akt, </span></span>MAPK<span><span>, Nanog<span><span>, STAT 3, and Wnt signaling pathways are involved in GBM progression and invasion. Besides, </span>biological processes<span><span> such as anti-apoptosis, autophagy, angiogenesis, and stemness promote GBM </span>malignancy<span>. Resveratrol<span> (RESV) is a non-flavonoid polyphenol with high antitumor activity, the potential of which, regulating signaling pathways involved in cancer malignancy, have been demonstrated by many studies. Herein, we present the potential of RESV in both single and combination therapy- targeting various signaling pathways- which induce apoptotic cell death, re-sensitize </span></span></span></span></span>cancer cells to radiotherapy, and induce chemo-sensitizing effects to eventually inhibit GBM progression.</span></span></p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10011412","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}

{"title":"PRSS2 regulates EMT and metastasis via MMP-9 in gastric cancer","authors":"Fei Wang ,&nbsp;Jianfeng Yi ,&nbsp;Yu Chen ,&nbsp;Xiang Bai ,&nbsp;Chunfeng Lu ,&nbsp;Shichun Feng ,&nbsp;Xiaojun Zhou","doi":"10.1016/j.acthis.2023.152071","DOIUrl":"10.1016/j.acthis.2023.152071","url":null,"abstract":"<div><p>Serine protease<span> 2 (PRSS2) is upregulated in gastric cancer tissues, correlates with poor prognosis and promotes migration and invasion of gastric cancer cells<span><span>. However, the exact mechanism by which PRSS2 promotes </span>metastasis<span><span> in gastric cancer is unclear. We examined serum PRSS2 levels in healthy controls and gastric cancer patients by enzyme linked immunosorbent assay (ELISA) and analyzed the correlation between PRSS2 serum level with the clinicopathological characteristics of gastric cancer patients and matrix metalloproteinase-9 (MMP-9) expression. A lentiviral MMP-9 overexpression vector was constructed and used to transfect gastric cancer cells with stable silencing of PRSS2, and migration, invasion and epithelial-mesenchymal transition (EMT) of gastric cancer cells were examined. High serum PRSS2 levels were detected in gastric cancer patients and associated with </span>lymphatic metastasis and TNM stage. Serum PRSS2 was positively correlated with serum MMP-9 level. PRSS2 silencing inhibited EMT, and knock-down of PRSS2 partially abrogated cell metastasis and EMT caused by overexpression of MMP-9. These results suggest that PRSS2 promotes the migration and invasion of gastric cancer cells through EMT induction by MMP-9. Our findings suggest that PRSS2 may be a potential early diagnostic marker and therapeutic target of gastric cancer.</span></span></span></p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9957217","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}

{"title":"Impacts of iron on ultrastructural features of NCI-H295R cell line related to steroidogenesis","authors":"Hana Duranova ,&nbsp;Veronika Fialkova ,&nbsp;Veronika Simora ,&nbsp;Jana Bilcikova ,&nbsp;Peter Massanyi ,&nbsp;Norbert Lukac ,&nbsp;Zuzana Knazicka","doi":"10.1016/j.acthis.2023.152056","DOIUrl":"10.1016/j.acthis.2023.152056","url":null,"abstract":"<div><p><span>The current study was intended to evaluate impacts of both iron (Fe) enrichment and overload (in the form of ferrous sulphate heptahydrate, FeSO</span>₄.7H₂O) on ultrastructural characteristics of human adrenocarcinoma NCI-H295R cell line. Here, the NCI-H295R cells were treated with 0, 3.90, and 1000 µM FeSO₄.7H₂<span><span><span>O, and consequently proceeded for purposes of ultrastructural studies. Micrographs taken under transmission </span>electron microscope (TEM) were investigated from the qualitative and quantitative (unbiased stereological approaches) aspects, and obtained findings were compared among the three groups of the cells. The ultrastructural features related to the steroidogenic process were found to be similar between the untreated and both Fe-exposed cell populations, with conspicuous mitochondria with well-defined lamellar </span>cristae<span><span> (creating clusters of varying sizes in the regions of increased energy demands) and concentric whorls of smooth endoplasmic reticulum (SER) being the most noticeable characteristics. The precise estimates of the component (volume, surface) fractions of the nucleus, mitochondria, and </span>lipid droplets (LDs), as well as of the nucleus/cytoplasm (N/C) ratio have revealed close similarities (P &gt; 0.05) in all cell groups investigated. Nonetheless, the low concentration of FeSO</span></span>₄.7H₂<span>O exhibited beneficial action on ultrastructural organization of the NCI-H295R cells. In effect, these cells were distinguished by mitochondria with smoother surfaces and clearer outlines, higher density of thin, parallel lamellar cristae (deeply extending into the mitochondrial matrix), and more widespread distribution of fine SER tubules as compared to the control ones, all of them suggesting higher level of energy requirements and metabolic activity, and more intensive rate of steroidogenesis. Interestingly, no obvious ultrastructural modifications were observed in the NCI-H295R cells treated with high FeSO</span>₄.7H₂O concentration. This finding can be linked to either an adaptive ultrastructural machinery of these cells to cope with the adverse effect of the element or to insufficient dose of FeSO₄.7H₂O (1000 µM) to induce ultrastructural signs of cytotoxicity. Purposefully, the results of the current study complement our previous paper dealing with impacts of FeSO₄.7H₂<span><span>O on the NCI-H295R cell viability and steroidogenesis at the molecular level. Hence, they fill a knowledge gap considering structure-function coupling in this </span>cellular model<span> system upon the metal exposure. This integrated approach can enhance our understanding of the cellular responses to Fe enrichment and overload which can be helpful for individuals with reproductive health concerns.</span></span></p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10329189","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}

{"title":"Study of platelet-rich fibrin promoting endothelial cell differentiation and angiogenesis induced by transplantation of adipose-derived stem cells","authors":"Zhibing Ma ,&nbsp;Jin Ding ,&nbsp;Yawen Wang ,&nbsp;Tianqi Zhang ,&nbsp;Gang Chen ,&nbsp;Jinlong Huang","doi":"10.1016/j.acthis.2023.152059","DOIUrl":"10.1016/j.acthis.2023.152059","url":null,"abstract":"<div><p>Diabetic patients are characterized by long wound healing time, and adipose stem cells (ADSCs) can secrete growth factors to promote angiogenesis and improve diabetic wound healing. In this research, we attempted to interrogate the impact of platelet-rich fibrin (PRF) on ADSCs in diabetic wound healing. ADSCs were harvested from human adipose tissues and identified through flow cytometry. After pretreatment with cultured medium supplemented with different concentrations of PRF (2.5%, 5%, and 7.5%), proliferation and differentiation capacity of ADSCs were assessed by CCK-8 assay, qRT-PCR and immunofluorescence (IF), respectively. Tube formation assay measured angiogenesis. Western blot analysis analyzed expression of endothelial markers and the extracellular signal-regulated kinase (ERK) and serine/threonine kinase (Akt) pathways in PRF-induced ADSCs. The CCK-8 experiment indicated that PRF enhanced proliferation of ADSCs in dose-dependent manner, relative to normal control group. The expression of endothelial markers and the capacity of tube formation were significantly promoted by 7.5% PRF. The release of growth factors containing vascular endothelial grow factor (VEGF) and insulin-like growth factor-1 (IGF-1) from PRF was increased with the extension of detection time. When the receptors of VEGF or/and IGF-1 were neutralized, ADSCs differentiation into endothelial cells were obviously inhibited. Additionally, PRF stimulated ERK and Akt pathways, and the inhibitors of ERK and Akt attenuated PRF-induced differentiation of ADSCs into endothelial cells. In conclusion, PRF promoted endothelial cell differentiation and angiogenesis induced by ADSCs in diabetic wound healing, which appears to give guidance for treating patients.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9957215","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}

{"title":"Astaxanthin inhibits oxidative stress and apoptosis in diabetic retinopathy","authors":"Jian Fang ,&nbsp;Wuxia Bai ,&nbsp;Lina Yang","doi":"10.1016/j.acthis.2023.152069","DOIUrl":"10.1016/j.acthis.2023.152069","url":null,"abstract":"<div><h3>Background</h3><p><span><span>The pathophysiology of </span>diabetic retinopathy<span> (DR) is thought to be influenced by oxidative stress. </span></span>Astaxanthin (ASX) is a natural product with antioxidant effect, but it is not clear whether its mechanism of inhibiting the development of DR is related to anti-oxidation.</p></div><div><h3>Methods</h3><p>Rats were intraperitoneally injected with streptozotocin<span><span><span> (60 mg/kg) to create DR rat models followed by ASX (20 mg/kg) for 45 days. Retinal tissue was examined by Hematoxylin<span> and Eosin staining. By using Enzyme-linked immunosorbent assay (ELISA), 2,7-Dichlorodrhydrofluorescein diace (DCFH-DA) probes, </span></span>immunohistochemistry<span> and western blot, it was feasible to evaluate the contents of inflammation-related factors (tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and macrophage inhibitory cytokine-1 (MIC-1)), oxidative stress-related indicators (glutathione (GSH), </span></span>malonic dialdehyde<span> (MDA), glutathione peroxidase<span> (GPx), reactive oxygen species<span><span><span> (ROS) and Total antioxidant capacity (T-AOC)), antioxidant enzymes (hemoxgenase-1(HO-1) and </span>Quinone </span>Oxidoreductase 1 (NQO1)), and apoptosis-related proteins (Bcl-2, Bcl2 Associated X Protein (BAX), and cleaved-caspase-3). Additionally, antioxidant proteins downstream of the nuclear factor E2 related factors (Nrf-2) pathway, expression levels of Nrf2/ Kelch-like ECH-associated protein 1(Keap 1) pathway-associated proteins, and nuclear and cytoplasmic levels of Nrf2 were assessed using immunohistochemistry, western blot, or quantitative real-time polymerase chain reaction (qRT-PCR).</span></span></span></span></p></div><div><h3>Results</h3><p>ASX alleviated retinal tissue damage by increasing overall retina thickness and ganglion cell layer (GCL) cell numbers and exerted the anti-inflammatory, anti-oxidative stress, and anti-apoptosis effects in DR rats. Additionally, ASX could inhibit the expression of Keap1, promote the transport of Nrf2 from cytoplasm to nucleus and facilitate the expressions of HO-1, NQO1, γ-glutamylcysteine synthetase, (γ-GCS) and GPx.</p></div><div><h3>Conclusion</h3><p>ASX exerted antioxidant effects through Nrf2/keap1 pathway, thereby alleviating apoptosis, inflammation, and oxidative stress in retinal tissues of DR rats.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10314517","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}

{"title":"Immunohistochemical analysis of the vimentin filaments in Sertoli cells is a powerful tool for the prediction of spermatogenic dysfunction","authors":"Hirokatsu Saito,&nbsp;Satoshi Yokota,&nbsp;Satoshi Kitajima","doi":"10.1016/j.acthis.2023.152046","DOIUrl":"10.1016/j.acthis.2023.152046","url":null,"abstract":"<div><p>The close interaction between male germ cells and Sertoli cells<span><span><span>, a type of somatic cell found in the </span>seminiferous tubules<span><span> of mammalian testis, is essential for the normal progression of </span>spermatogenesis in mammals. </span></span>Vimentin<span><span><span> is an intermediate filament protein that primarily provides mechanical support, preserves cell shape, and maintains the nuclear position, and it is often used as a marker to identify Sertoli cells. Vimentin is known to be involved in many </span>diseases and aging processes; however, how vimentin is related to spermatogenic dysfunction and the associated functional changes is still unclear. In a previous study, we reported that </span>vitamin E<span><span><span> deficiency affected the testes, epididymis<span>, and spermatozoa of mice, accelerating the progression of senescence. In this study, we focused on the Sertoli cell marker vimentin and explored the relationship between the cytoskeletal system of Sertoli cells and spermatogenic dysfunction using </span></span>testis tissue<span> sections that caused male reproductive dysfunction with vitamin E deficiency. The immunohistochemical analysis showed that the proportion of the vimentin-positive area in seminiferous tubule cross-sections was significantly increased in testis tissue sections of the vitamin E-deficient group compared with the proportion in the control group. The histological analysis of testis tissue sections from the vitamin E-deficient group showed that vimentin-positive Sertoli cells were greatly extended from the </span></span>basement membrane, along with an increased abundance of vimentin. These findings suggest that vimentin may be a potential indicator for detecting spermatogenic dysfunction.</span></span></span></p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10016345","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}