European Journal of Histochemistry最新文献

{"title":"Substance P is overexpressed in cervical squamous cell carcinoma and promoted proliferation and invasion of cervical cancer cells <em>in vitro</em>.","authors":"Ying Wang, Shifa Yuan, Jing Ma, Hong Liu, Lizhen Huang, Fengzhen Zhang","doi":"10.4081/ejh.2023.3746","DOIUrl":"10.4081/ejh.2023.3746","url":null,"abstract":"<p><p>This study aimed to investigate the expression and function of substance P in cervical squamous cell carcinoma. Cancer tissues and adjacent tissues of 20 patients with cervical squamous cell carcinoma in our hospital were collected. The expression of substance P was detected by immunohistochemistry and Western blot analysis. Cervical squamous cell carcinoma line SiHa was treated with different concentrations of substance P. The proliferation of SiHa cells was detected by EdU assay, and the invasion ability of SiHa cells was detected by transwell assay. The phosphorylation of ERK1/2 and the expression of MMP9 were detected by Western blot analysis. The results showed that substance P was expressed in the cytoplasm and some cell membranes of cervical squamous cell carcinoma cells. The expression of substance P in cervical cancer tissues was significantly higher than that in the adjacent tissues. Compared with the control group, substance P significantly promoted the proliferation and invasion of SiHa cells in a concentration dependent manner and activated the phosphorylation of ERK1/2 and upregulated the expression of MMP9 in SiHa cells. In conclusion, substance P is highly expressed in cervical squamous cell carcinoma and can promote cervical cancer cell proliferation and invasion. The mechanism is related to the activation of ERK1/2 pathway to upregulate MMP9.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 3","pages":""},"PeriodicalIF":2.1,"publicationDate":"2023-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/43/43/ejh-67-3-3746.PMC10476533.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10215094","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}

{"title":"Therapeutic effects of human umbilical cord mesenchymal stem cell-derived extracellular vesicles on ovarian functions through the PI3K/Akt cascade in mice with premature ovarian failure.","authors":"Nan Li,&nbsp;Xue Fan,&nbsp;Lihong Liu,&nbsp;Yanbing Liu","doi":"10.4081/ejh.2023.3506","DOIUrl":"https://doi.org/10.4081/ejh.2023.3506","url":null,"abstract":"<p><p>Premature ovarian failure (POF) mainly refers to ovarian dysfunction in females younger than forty. Mesenchymal stem cells (MSCs) are considered an increasingly promising therapy for POF. This study intended to uncover the therapeutic effects of human umbilical cord MSC-derived extracellular vesicles (hucMSCEVs) on POF. hucMSCs were identified by observing morphology and examining differentiation capabilities. EVs were extracted from hucMSCs and later identified utilizing nanoparticle tracking analysis, transmission electron microscopy, and Western blotting. POF mouse models were established by injecting D-galactose (Dgal). The estrous cycles were assessed through vaginal cytology, and serum levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), anti-mullerian hormone (AMH), estradiol (E2), and progesterone (P) were measured by ELISA. The human ovarian granulosa cell line KGN was used for in vitro experiments. The uptake of hucMSC-EVs by KGN cells was detected. After D-gal treatment, cell proliferation and apoptosis were assessed via CCK-8 assay and flow cytometry. The PI3K/Akt pathway-related proteins were determined by Western blotting. Our results revealed that POF mice had prolonged estrous cycles, increased FSH and LH levels, and decreased AMH, E2, and P levels. Treatment with hucMSC-EVs partially counteracted the above changes. D-gal treatment reduced proliferation and raised apoptosis in KGN cells, while hucMSC-EV treatment annulled the changes. D-gal-treated cells exhibited downregulated p-PI3K/PI3K and p-Akt/Akt levels, while hucMSC-EVs activated the PI3K/Akt pathway. LY294002 suppressed the roles of hucMSC-EVs in promoting KGN cell proliferation and lowering apoptosis. Collectively, hucMSC-EVs facilitate proliferation and suppress apoptosis of ovarian granulosa cells by activating the PI3K/Akt pathway, thereby alleviating POF.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 3","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b5/ce/ejh-67-3-3506.PMC10476539.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10156699","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}

{"title":"Deletion of osteopontin in non-small cell lung cancer cells affects bone metabolism by regulating miR-34c/Notch1 axis: a clue to bone metastasis.","authors":"Jing Guo,&nbsp;Chang-Yong Tong,&nbsp;Jian-Guang Shi,&nbsp;Xin-Jian Li,&nbsp;Xue-Qin Chen","doi":"10.4081/ejh.2023.3631","DOIUrl":"https://doi.org/10.4081/ejh.2023.3631","url":null,"abstract":"<p><p>Lung cancer is prone to bone metastasis, and osteopontin (OPN) has an important significance in maintaining bone homeostasis. The goal of this study was to explore the impact of OPN level on bone metabolism and the molecular mechanism of inhibiting bone metastasis in non-small cell lung cancer (NSCLC). The expression of OPN in NSCLC was ascertained by Western blot and immunohistochemistry, and the correlation between the expression level of OPN and survival of patients was analyzed. Then the shRNA technology was applied to reduce the expression of OPN in NSCLC cells, and CCK-8 assay was carried out to investigate the effect of low expression of OPN on the proliferation of NSCLC cells. In addition, the effects of low expression of OPN on osteoclast differentiation, osteoblast generation and mineralization were studied using osteoclast precursor RAW264.7 and human osteoblast SaOS-2 cells, and whether OPN could regulate miR-34c/ Notch pathway to affect bone metabolism was further explored. The findings showed that the high level of OPN in NSCLC was closely related to the poor prognosis of patients and the abnormal proliferation of NSCLC cell lines. The suppression of OPN was beneficial to inhibit the differentiation of osteoclasts and promote the mineralization of osteoblasts. Besides, this study confirmed that the deletion of OPN can regulate bone metabolism through the regulation of miR-34c/Notch1 pathway, which will contribute to inhibiting the occurrence of osteolytic bone metastasis in NSCLC.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 3","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c9/09/ejh-67-3-3631.PMC10476534.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10150310","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}

{"title":"Dexmedetomidine attenuates neuroinflammation and microglia activation in LPS-stimulated BV2 microglia cells through targeting circ-Shank3/miR-140-3p/TLR4 axis.","authors":"Guangbao He,&nbsp;Yibo He,&nbsp;Hongwei Ni,&nbsp;Kai Wang,&nbsp;Yijun Zhu,&nbsp;Yang Bao","doi":"10.4081/ejh.2023.3766","DOIUrl":"https://doi.org/10.4081/ejh.2023.3766","url":null,"abstract":"<p><p>It has been shown that dexmedetomidine (Dex) could attenuate postoperative cognitive dysfunction (POCD) via targeting circular RNAs (circRNAs). Circ-Shank3 has been found to be involved in the neuroprotective effects of Dex against POCD. However, the role of circ-Shank3 in POCD remains largely unknown. Reverse transcription quantitative PCR (RT-qPCR) was performed to detect circ-Shank3 and miR-140-3p levels in lipopolysaccharide (LPS)-treated microglia BV-2 cells in the absence or presence of Dex. The relationship among circ-Shank3, miR-140-3p and TLR4 was confirmed by dual-luciferase reporter assay. Additionally, Western blot and immunofluorescence (IF) assays were conducted to evaluate TLR4, p65 and Iba-1 or CD11b levels in cells. In this study, we found that Dex notably decreased circ-Shank3 and TLR4 levels and elevated miR-140-3p level in LPS-treated BV2 cells. Mechanistically, circ-Shank3 harbor miR-140-3p, functioning as a miRNA sponge, and then miR-140-3p targeted the 3'-UTR of TLR4. Additionally, Dex treatment significantly reduced TLR4 level and phosphorylation of p65, and decreased the expressions of microglia markers Iba-1 and CD11b in LPS-treated BV2 cells. As expected, silenced circ-Shank3 further reduced TLR4, p65 and Iba-1 and CD11b levels in LPS-treated BV2 cells in the presence of Dex, whereas these phenomena were reversed by miR-140-3p inhibitor. Collectively, our results found that Dex could attenuate the neuroinflammation and microglia activation in BV2 cells exposed to LPS via targeting circ-Shank3/miR-140-3p/TLR4 axis. Our results might shed a new light on the mechanism of Dex for the treatment of POCD.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 3","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0b/f9/ejh-67-3-3766.PMC10476535.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10158089","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}

{"title":"LncRNA FBXO18-AS promotes gastric cancer progression by TGF-β1/Smad signaling.","authors":"Yiming Zhang,&nbsp;Wanqiong Zheng,&nbsp;Liang Zhang,&nbsp;Yechun Gu,&nbsp;Lihe Zhu,&nbsp;Yingpeng Huang","doi":"10.4081/ejh.2023.3667","DOIUrl":"https://doi.org/10.4081/ejh.2023.3667","url":null,"abstract":"<p><p>For the digestive system, there exists one common malignant tumor, known as gastric cancer. It is the third most prevalent type of tumor among different tumors worldwide. It has been reported that long noncoding RNAs (lncRNAs), participate in various biological processes of gastric cancer. However, there are still many lncRNAs with unknown functions, and we discovered a novel lncRNA designated as FBXO18-AS. Whether lncRNAFBXO18-AS participates in gastric cancer progression is still unknown. Bioinformatic analysis, immunohistochemistry, Western blotting, and qPCR were carried out to explore FBXO18-AS and TGF-β1 expression. In addition, EdU, MTS, migration and transwell assays were performed to investigate the invasion, proliferation and migration of gastric cancer in vitro. We first discovered that FBXO18-AS expression was upregulated in gastric cancer and linked to poorer outcomes among patients with gastric cancer. Then, we confirmed that FBXO18-AS promoted the proliferation, invasion, migration, and an EMT-like process in gastric cancer in vivo and in vitro. Mechanistically, FBXO18-AS was found to be involved in the progression of gastric cancer by modulating TGF-β1/Smad signaling. Therefore, it might offer a possible biomarker for gastric cancer diagnosis and an effective strategy for clinical treatment.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/99/81/ejh-67-2-3667.PMC10334307.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9829062","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}

{"title":"Erratum - Transcription factor nuclear factor erythroid 2 p45-related factor 2 (NRF2) ameliorates sepsis-associated acute kidney injury by maintaining mitochondrial homeostasis and improving the mitochondrial function.","authors":"Zhijiang Chen,&nbsp;Huili Wang,&nbsp;Bin Hu,&nbsp;Xinxin Chen,&nbsp;Meiyu Zheng,&nbsp;Lili Liang,&nbsp;Juanjuan Lyu,&nbsp;Qiyi Zeng","doi":"10.4081/ejh.2023.3794","DOIUrl":"https://doi.org/10.4081/ejh.2023.3794","url":null,"abstract":"<p><p>This corrects the article published in European Journal of Histochemistry 2022;66:3412. doi: 10.4081/ejh.2022.3412.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d2/81/ejh-67-2-3794.PMC10334305.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9829060","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}

{"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":"<p><p>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.</p>","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}

{"title":"LncRNA gadd7 promotes mitochondrial membrane potential decrease and apoptosis of alveolar type II epithelial cells by positively regulating MFN1 in an <i>in vitro</i> 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":"<p><p>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.</p>","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}

{"title":"Proceedings of the workshop NANO23@uniVR - 8-9 June 2023, University of Verona, Italy.","authors":"The Scientific Committee","doi":"10.4081/ejh.2023.3778","DOIUrl":"10.4081/ejh.2023.3778","url":null,"abstract":"<p><p>The workshop, organized by the PhD Course in Nanosciences and Advanced Technologies, aims to create a forum on hot topics of current interest in Nanoscience and Nanotechnology such as Nanomedicine, Biotechnology, Energy-nanotech, Environmental nanoscience, Green nanotechnology, Nanoengineering.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"1 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41537572","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":"Metformin sensitises osteosarcoma to chemotherapy <em>via</em> the IGF-1R/miR-610/FEN1 pathway.","authors":"Suwei Dong,&nbsp;Yanbin Xiao,&nbsp;Ziqiang Zhu,&nbsp;Xiang Ma,&nbsp;Zhuohui Peng,&nbsp;Jianping Kang,&nbsp;Jianqiang Wang,&nbsp;Yunqing Wang,&nbsp;Zhen Li","doi":"10.4081/ejh.2023.3612","DOIUrl":"https://doi.org/10.4081/ejh.2023.3612","url":null,"abstract":"<p><p>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.</p>","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}