European Journal of Histochemistry最新文献_第9页

Sodium hyaluronate promotes proliferation, autophagy, and migration of corneal epithelial cells by downregulating miR-18a in the course of corneal epithelial injury. 在角膜上皮损伤过程中，透明质酸钠通过下调 miR-18a 促进角膜上皮细胞的增殖、自噬和迁移。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2023-06-15 DOI: 10.4081/ejh.2023.3663

Yingzhuo Guo, Hua Wang

{"title":"Sodium hyaluronate promotes proliferation, autophagy, and migration of corneal epithelial cells by downregulating miR-18a in the course of corneal epithelial injury.","authors":"Yingzhuo Guo, Hua Wang","doi":"10.4081/ejh.2023.3663","DOIUrl":"10.4081/ejh.2023.3663","url":null,"abstract":"Corneal epithelium can resist the invasion of external pathogenic factors to protect the eye from external pathogens. Sodium hyaluronate (SH) has been confirmed to promote corneal epithelial wound healing. However, the mechanism by which SH protects against corneal epithelial injury (CEI) is not fully understood. CEI model mice were made by scratching the mouse corneal epithelium, and in vitro model of CEI were constructed via curettage of corneal epithelium or ultraviolet radiation. The pathologic structure and level of connective tissue growth factor (CTGF) expression were confirmed by Hematoxylin and Eosin staining and immunohistochemistry. CTGF expression was detected by an IHC assay. The levels of CTGF, TGF-β, COLA1A, FN, LC3B, Beclin1, and P62 expression were monitored by RT-qPCR, ELISA, Western blotting or immunofluorescence staining. Cell proliferation was detected by the CCK-8 assay and EdU staining. Our results showed that SH could markedly upregulate CTGF expression and downregulate miR-18a expression in the CEI model mice. Additionally, SH could attenuate corneal epithelial tissue injury, and enhance the cell proliferation and autophagy pathways in the CEI model mice. Meanwhile, overexpression of miR-18a reversed the effect of SHs on cell proliferation and autophagy in CEI model mice. Moreover, our data showed that SH could induce the proliferation, autophagy, and migration of CEI model cells by downregulating miR-18a. Down-regulation of miR-18a plays a significant role in the ability of SH to promote corneal epithelial wound healing. Our results provide a theoretical basis for targeting miR-18a to promote corneal wound healing.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2023-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7f/0a/ejh-67-2-3663.PMC10334306.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9772350","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}

引用次数: 0

LncRNA gadd7 promotes mitochondrial membrane potential decrease and apoptosis of alveolar type II epithelial cells by positively regulating MFN1 in an in vitro model of hyperoxia-induced acute lung injury. 在体外高氧诱导急性肺损伤模型中，LncRNA gadd7通过正向调节MFN1促进线粒体膜电位下降和肺泡II型上皮细胞凋亡。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2023-05-31 DOI: 10.4081/ejh.2023.3535

Guoyue Liu, Cunzhi Yin, Mingjiang Qian, Xuan Xiao, Hang Wu, Fujian Fu

{"title":"LncRNA gadd7 promotes mitochondrial membrane potential decrease and apoptosis of alveolar type II epithelial cells by positively regulating MFN1 in an in vitro model of hyperoxia-induced acute lung injury.","authors":"Guoyue Liu, Cunzhi Yin, Mingjiang Qian, Xuan Xiao, Hang Wu, Fujian Fu","doi":"10.4081/ejh.2023.3535","DOIUrl":"10.4081/ejh.2023.3535","url":null,"abstract":"The mortality and morbidity rates of ovarian cancer (OC) are high, but the underlying mechanisms of OC have not been characterized. In this study, we determined the role of Rho GTPase Activating Protein 30 (ARHGAP30) in OC progression. We measured ARHGAP30 abundance in OC tissue samples and cells using immunohistochemistry (IHC) and RT-qPCR. EdU, transwell, and annexin V/PI apoptosis assays were used to evaluate proliferation, invasiveness, and apoptosis of OC cells, respectively. The results showed that ARHGAP30 was overexpressed in OC tissue samples and cells. Inhibition of ARHGAP30 suppressed growth and metastasis of OC cells, and enhanced apoptosis. Knockdown of ARHGAP30 in OC cells significantly inhibited the PI3K/AKT/mTOR pathway. Treatment with the PI3K/AKT/mTOR pathway inhibitor buparlisib simulated the effects of ARHGAP30 knockdown on growth, invasiveness, and apoptosis of OC cells. Following buparlisib treatment, the expression levels of p-PI3K, p-AKT, and p-mTOR were significantly decreased. Furthermore, buparlisib inhibited the effects of ARHGAP30 upregulation on OC cell growth and invasiveness. In conclusion, ARHGAP30 regulated the PI3K/AKT/mTOR pathway to promote progression of OC.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2023-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0e/58/ejh-67-2-3535.PMC10277814.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9670965","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}

引用次数: 0

Proceedings of the workshop NANO23@uniVR - 8-9 June 2023, University of Verona, Italy. 研讨会记录NANO23@uniVR-2023年6月8日至9日，意大利维罗纳大学

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-05-31 DOI: 10.4081/ejh.2023.3778

The Scientific Committee

引用次数: 0

Metformin sensitises osteosarcoma to chemotherapy via the IGF-1R/miR-610/FEN1 pathway. 二甲双胍通过IGF-1R/miR-610/FEN1通路使骨肉瘤对化疗敏感。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-05-17 DOI: 10.4081/ejh.2023.3612

Suwei Dong, Yanbin Xiao, Ziqiang Zhu, Xiang Ma, Zhuohui Peng, Jianping Kang, Jianqiang Wang, Yunqing Wang, Zhen Li

{"title":"Metformin sensitises osteosarcoma to chemotherapy via the IGF-1R/miR-610/FEN1 pathway.","authors":"Suwei Dong, Yanbin Xiao, Ziqiang Zhu, Xiang Ma, Zhuohui Peng, Jianping Kang, Jianqiang Wang, Yunqing Wang, Zhen Li","doi":"10.4081/ejh.2023.3612","DOIUrl":"https://doi.org/10.4081/ejh.2023.3612","url":null,"abstract":"Metformin can enhance cancer cell chemosensitivity to anticancer drugs. IGF-1R is involved in cancer chemoresistance. The current study aimed to elucidate the role of metformin in osteosarcoma (OS) cell chemosensitivity modulation and identify its underlying mechanism in IGF-1R/miR-610/FEN1 signalling. IGF-1R, miR-610, and FEN1 were aberrantly expressed in OS and participated in apoptosis modulation; this effect was abated by metformin treatment. Luciferase reporter assays confirmed that FEN1 is a direct target of miR-610. Moreover, metformin treatment decreased IGF-1R and FEN1 but elevated miR-610 expression. Metformin sensitised OS cells to cytotoxic agents, while FEN1 overexpression partly compromised metformin's sensitising effects. Furthermore, metformin was observed to enhance adriamycin's effects in a murine xenograft model. Metformin enhanced OS cell sensitivity to cytotoxic agents via the IGF-1R/miR-610/FEN1 signalling axis, highlighting its potential as an adjuvant during chemotherapy.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/47/7c/ejh-67-2-3612.PMC10230554.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9563915","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}

引用次数: 0

High glucose inhibits neural differentiation by excessive autophagy via peroxisome proliferator-activated receptor gamma. 高糖通过过氧化物酶体增殖物激活受体γ通过过度自噬抑制神经分化。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-05-11 DOI: 10.4081/ejh.2023.3691

Yin Pan, Di Qiu, Shu Chen, Xiaoxue Han, Ruiman Li

{"title":"High glucose inhibits neural differentiation by excessive autophagy via peroxisome proliferator-activated receptor gamma.","authors":"Yin Pan, Di Qiu, Shu Chen, Xiaoxue Han, Ruiman Li","doi":"10.4081/ejh.2023.3691","DOIUrl":"https://doi.org/10.4081/ejh.2023.3691","url":null,"abstract":"The high prevalence of prediabetes and diabetes globally has led to the widespread occurrence of severe complications, such as diabetic neuropathy, which is a result of chronic hyperglycemia. Studies have demonstrated that maternal diabetes can lead to neural tube defects by suppressing neurogenesis during neuroepithelium development. While aberrant autophagy has been associated with abnormal neuronal differentiation, the mechanism by which high glucose suppresses neural differentiation in stem cells remains unclear. Therefore, we developed a neuronal cell differentiation model of retinoic acid induced P19 cells to investigate the impact of high glucose on neuronal differentiation in vitro. Our findings indicate that high glucose (HG) hinders neuronal differentiation and triggers excessive. Furthermore, HG treatment significantly reduces the expression of markers for neurons (Tuj1) and glia (GFAP), while enhancing autophagic activity mediated by peroxisome proliferator-activated receptor gamma (PPARγ). By manipulating PPARγ activity through pharmacological approaches and genetically knocking it down using shRNA, we discovered that altering PPARγ activity affects the differentiation of neural stem cells exposed to HG. Our study reveals that PPARγ acts as a downstream mediator in high glucose-suppressed neural stem cell differentiation and that refining autophagic activity via PPARγ at an appropriate level could improve neuronal differentiation efficiency. Our data provide novel insights and potential therapeutic targets for the clinical management of gestational diabetes mellitus.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/3e/19/ejh-67-2-3691.PMC10230556.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9931775","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}

引用次数: 1

Knockdown of ARHGAP30 inhibits ovarian cancer cell proliferation, migration, and invasiveness by suppressing the PI3K/AKT/mTOR signaling pathway. 敲低ARHGAP30通过抑制PI3K/AKT/mTOR信号通路抑制卵巢癌细胞的增殖、迁移和侵袭性。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-05-11 DOI: 10.4081/ejh.2023.3653

Xiaoyan Chu, Jun Lou, Yun Yi, Linlin Zhong, Ouping Huang

{"title":"Knockdown of ARHGAP30 inhibits ovarian cancer cell proliferation, migration, and invasiveness by suppressing the PI3K/AKT/mTOR signaling pathway.","authors":"Xiaoyan Chu, Jun Lou, Yun Yi, Linlin Zhong, Ouping Huang","doi":"10.4081/ejh.2023.3653","DOIUrl":"https://doi.org/10.4081/ejh.2023.3653","url":null,"abstract":"The mortality and morbidity rates of ovarian cancer (OC) are high, but the underlying mechanisms of OC have not been characterized. In this study, we determined the role of Rho GTPase Activating Protein 30 (ARHGAP30) in OC progression. We measured ARHGAP30 abundance in OC tissue samples and cells using immunohistochemistry (IHC) and RT-qPCR. EdU, transwell, and annexin V/PI apoptosis assays were used to evaluate proliferation, invasiveness, and apoptosis of OC cells, respectively. The results showed that ARHGAP30 was overexpressed in OC tissue samples and cells. Inhibition of ARHGAP30 suppressed growth and metastasis of OC cells, and enhanced apoptosis. Knockdown of ARHGAP30 in OC cells significantly inhibited the PI3K/AKT/mTOR pathway. Treatment with the PI3K/AKT/mTOR pathway inhibitor buparlisib simulated the effects of ARHGAP30 knockdown on growth, invasiveness, and apoptosis of OC cells. Following buparlisib treatment, the expression levels of p-PI3K, p-AKT, and p-mTOR were significantly decreased. Furthermore, buparlisib inhibited the effects of ARHGAP30 upregulation on OC cell growth and invasiveness. In conclusion, ARHGAP30 regulated the PI3K/AKT/mTOR pathway to promote progression of OC.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/3b/42/ejh-67-2-3653.PMC10230553.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9559623","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}

引用次数: 0

RETRACTION: Intrinsic innervation and dopaminergic markers after experimental denervation in rat thymus. 收缩:实验性胸腺去神经后的内在神经支配和多巴胺能标记物。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-05-08 DOI: 10.4081/ejh.2023.3765

Fiorenzo Mignini, Maurizio Sabbatini, Vito D'Andrea, Carlo Cavallotti

{"title":"RETRACTION: Intrinsic innervation and dopaminergic markers after experimental denervation in rat thymus.","authors":"Fiorenzo Mignini, Maurizio Sabbatini, Vito D'Andrea, Carlo Cavallotti","doi":"10.4081/ejh.2023.3765","DOIUrl":"https://doi.org/10.4081/ejh.2023.3765","url":null,"abstract":"On behalf of the coauthors and with much regret, I must retract our publication entitled \"Intrinsic innervation and dopaminergic markers after experimental denervation in rat thymus\" published in European Journal of Histochemistry 2010;54(2):e17 for the following reason: Unfortunately, now, after thirteen years, we have realized that some microphotographs published in the paper have been processed to improve the presentation of the images. The three surviving authors of the paper agree that the processing of the presentation images is against the COPE Ethical Editorial Standard, although the presentation images do not alter the integrity of methodological procedures and the results of the research work, obtained from the direct analysis of slides under microscope and rigorous statistical analysis of data; therefore, we, the authors of the above indicated paper, request the retraction of the publication. We apologize for what happened. Maurizio Sabbatini Dip. di Scienze e Innovazione Tecnologica (DISIT) Università del Piemonte Orientale Alessandria, Italy.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a2/17/ejh-67-2-3765.PMC10203977.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9519597","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}

引用次数: 0

The role of miR-143-3p/FNDC1 axis on the progression of non-small cell lung cancer. miR-143-3p/FNDC1轴在非小细胞肺癌进展中的作用

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-05-03 DOI: 10.4081/ejh.2023.3577

Zhanshu Ma, Qi Gao, Wenjing Xin, Lei Wang, Yan Chen, Chang Su, Songyan Gao, Ruiling Sun

{"title":"The role of miR-143-3p/FNDC1 axis on the progression of non-small cell lung cancer.","authors":"Zhanshu Ma, Qi Gao, Wenjing Xin, Lei Wang, Yan Chen, Chang Su, Songyan Gao, Ruiling Sun","doi":"10.4081/ejh.2023.3577","DOIUrl":"https://doi.org/10.4081/ejh.2023.3577","url":null,"abstract":"The study aimed to explore the functional role of fibronectin type III domain containing 1 (FNDC1) in nonsmall cell lung cancer (NSCLC), as well as the mechanism governing its expression. The expression levels of FNDC1 and related genes in tissue and cell samples were detected by qRT-PCR. Kaplan-Meier analysis was employed to analyze the association between FNDC1 level and the overall survival of NSCLC patients. Functional experiments such as CCK-8 proliferation, colony formation, EDU staining, migration and invasion assays were conducted to investigate the functional role of FNDC1 in regulating the malignancy of NSCLC cells. Bioinformatic tools and dual-luciferase reporter assay were used to identify the miRNA regulator of FNDC1 in NSCLC cells. Our data revealed the upregulation of FNDC1 at mRNA and protein levels in NSCLC tumor tissues cancer cell lines, compared with normal counterparts. NSCLC patients with higher FNDC1 expression suffered from a poorer overall survival. FNDC1 knockdown significantly suppressed the proliferation, migration and invasion of NSCLC cells, and had an inhibitory effect on tube formation. We further demonstrated that miR-143-3p was an upstream regulator of FNDC1 and miR-143-3p expression was repressed in NSCLC samples. Similar to FNDC1 knockdown, miR-143-3p overexpression inhibited the growth, migration and invasion of NSCLC cells. FNDC1 overexpression could partially rescue the effect of miR-143-3p overexpression. FNDC1 silencing also suppressed the tumorigenesis of NSCLC cells in mouse model. In conclusion, FNDC1 promotes the malignant prototypes of NSCLC cells. miR-143-3p is a negative regulator of FNDC1 in NSCLC cells, which may serve as a promising therapeutic target in NSCLC.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4a/43/ejh-67-2-3577.PMC10203978.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10299164","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}

引用次数: 1

Clinicopathological assessment of PD-1/PD-L1 immune checkpoint expression in desmoid tumors. 硬纤维瘤中PD-1/PD-L1免疫检查点表达的临床病理评价。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-04-26 DOI: 10.4081/ejh.2023.3688

Kazuhiko Hashimoto, Shunji Nishimura, Yu Shinyashiki, Tomohiko Ito, Ryosuke Kakinoki, Masao Akagi

{"title":"Clinicopathological assessment of PD-1/PD-L1 immune checkpoint expression in desmoid tumors.","authors":"Kazuhiko Hashimoto, Shunji Nishimura, Yu Shinyashiki, Tomohiko Ito, Ryosuke Kakinoki, Masao Akagi","doi":"10.4081/ejh.2023.3688","DOIUrl":"https://doi.org/10.4081/ejh.2023.3688","url":null,"abstract":"The details of immune molecules' expression in desmoid tumors (DTs) remain unclear. This study aimed to determine the expression status of the programmed death-1/programmed death ligand 1 (PD1/PD-L1) immune checkpoint mechanism in DTs. The study included patients with DTs (n=9) treated at our institution between April 2006 and December 2012. Immunostaining for CD4, CD8, PD-1, PD-L1, interleukin-2 (IL-2), and interferon-gamma (IFN-γ) was performed on pathological specimens harvested during the biopsy. The positivity rate of each immune component was calculated as the number of positive cells/total cells. The positivity rate was quantified and correlations between the positivity rates of each immune molecule were also investigated. Immune molecules other than PD-1 were stained in tumor cells and intra-tumor infiltrating lymphocytes. The mean ± SD expression rates of β-catenin, CD4, CD8, PD-1, PD-L1, IL-2, and IFN-ɤ were 43.9±18.9, 14.6±6.80, 0.75±4.70, 0±0, 5.1±6.73, 8.75±6.38, and 7.03±12.1, respectively. The correlation between β-catenin and CD4 was positively moderate (r=0.49); β-catenin and PD-L1, positively weak (r=0.25); CD4 and PD-L1, positively medium (r=0.36); CD8 and IL-2, positively medium (r=0.38); CD8 and IFN-ɤ, positively weak (r=0.28); and IL-2 and IFN-ɤ, positively medium (r=0.36). Our findings suggest that PD-L1-centered immune checkpoint mechanisms may be involved in the tumor microenvironment of DTs.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e7/df/ejh-67-2-3688.PMC10184173.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9467135","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}

引用次数: 1

Molecules involved in the sperm interaction in the human uterine tube: a histochemical and immunohistochemical approach. 参与精子在人输卵管中相互作用的分子:组织化学和免疫组织化学方法。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-04-13 DOI: 10.4081/ejh.2023.3513

David Cajas, Emanuel Guajardo, Sergio Jara-Rosales, Claudio Nuñez, Renato Vargas, Victor Carriel, Antonio Campos, Luis Milla, Pedro Orihuela, Carlos Godoy-Guzman

{"title":"Molecules involved in the sperm interaction in the human uterine tube: a histochemical and immunohistochemical approach.","authors":"David Cajas, Emanuel Guajardo, Sergio Jara-Rosales, Claudio Nuñez, Renato Vargas, Victor Carriel, Antonio Campos, Luis Milla, Pedro Orihuela, Carlos Godoy-Guzman","doi":"10.4081/ejh.2023.3513","DOIUrl":"https://doi.org/10.4081/ejh.2023.3513","url":null,"abstract":"In humans, even where millions of spermatozoa are deposited upon ejaculation in the vagina, only a few thousand enter the uterine tube (UT). Sperm transiently adhere to the epithelial cells lining the isthmus reservoir, and this interaction is essential in coordinating the availability of functional spermatozoa for fertilization. The binding of spermatozoa to the UT epithelium (mucosa) occurs due to interactions between cell-adhesion molecules on the cell surfaces of both the sperm and the epithelial cell. However, in humans, there is little information about the molecules involved. The aim of this study was to perform a histological characterization of the UT focused on determining the tissue distribution and deposition of some molecules associated with cell adhesion (F-spondin, galectin-9, osteopontin, integrin αV/β3) and UT's contractile activity (TNFα-R1, TNFα-R2) in the follicular and luteal phases. Our results showed the presence of galectin-9, F-spondin, osteopontin, integrin αV/β3, TNFα-R1, and TNFα-R2 in the epithelial cells in ampullar and isthmic segments during the menstrual cycle. Our results suggest that these molecules could form part of the sperm-UT interactions. Future studies will shed light on the specific role of each of the identified molecules.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/82/4d/ejh-67-2-3513.PMC10141343.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9361292","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}

引用次数: 0