Journal of Molecular Histology最新文献

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piR-38,736 promotes gastric cancer cell proliferation by downregulating SMAD4 expression
IF 2.9 4区 生物学
Journal of Molecular Histology Pub Date : 2025-04-03 DOI: 10.1007/s10735-025-10412-8
Dongmei Liu, Chenghai Wang, Hongshan Ge, Hong Yu
{"title":"piR-38,736 promotes gastric cancer cell proliferation by downregulating SMAD4 expression","authors":"Dongmei Liu,&nbsp;Chenghai Wang,&nbsp;Hongshan Ge,&nbsp;Hong Yu","doi":"10.1007/s10735-025-10412-8","DOIUrl":"10.1007/s10735-025-10412-8","url":null,"abstract":"<div><p>PIWI-interacting RNAs (piRNAs) play an important role in cancer development and progression. Although recent studies had advanced our understanding of the functions of various piRNAs in cancer, the specific role of piR-38736 in gastric cancer remained poorly understood. This study aimed to investigate the clinical significance and underlying mechanisms of piR-38736 in gastric cancer. This study found that piR-38736 was significantly upregulated in gastric cancer cells and tissues. Positive piR-38736 expression was closely correlated with larger tumor size and medium to poor differentiation. Survival analysis revealed that patients with positive piR-38736 expression had significantly shorter survival times compared to those with negative expression. Knockdown of piR-38736 markedly inhibited cell proliferation and tumor growth in gastric cancer. Furthermore, piR-38736 was found to directly bind to the 3′ untranslated region (UTR) of SMAD4 mRNA, resulting in significant downregulation of SMAD4 at both the mRNA and protein levels upon overexpression of piR-38,736. In conclusion, these findings indicate that piR-38,736 promotes cell proliferation and tumor growth in gastric cancer by downregulating SMAD4 expression. piR-38,736 may serve as a prognostic biomarker and a potential therapeutic target for gastric cancer. Further studies are required to fully elucidate the underlying mechanisms of piR-38,736 and explore its clinical implications in gastric cancer management.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-025-10412-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761728","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
PBK as a novel biomarker performed excellent diagnostic and prognostic value in HCC associated with immune infiltration and methylation
IF 2.9 4区 生物学
Journal of Molecular Histology Pub Date : 2025-04-03 DOI: 10.1007/s10735-024-10324-z
Beibei Lv, Fenna Zhang, Xinyi Zhang, Ziyi Wang, Shuai Hao, Na Ye, Na He
{"title":"PBK as a novel biomarker performed excellent diagnostic and prognostic value in HCC associated with immune infiltration and methylation","authors":"Beibei Lv,&nbsp;Fenna Zhang,&nbsp;Xinyi Zhang,&nbsp;Ziyi Wang,&nbsp;Shuai Hao,&nbsp;Na Ye,&nbsp;Na He","doi":"10.1007/s10735-024-10324-z","DOIUrl":"10.1007/s10735-024-10324-z","url":null,"abstract":"<div><p>Diagnostic and prognosis of hepatocellular carcinoma (HCC) remain major challenge in clinic. This study aimed to explore a gene signature for diagnosis and prognosis prediction of HCC followed by mechanism investigation. Differentially expressed genes (DEGs) in HCC were screened using TCGA. With specific formula, clinic features of prognosis associated DEGs were calculated to obtained a specific model followed by Kaplan–Meier analysis. Protein–protein interaction (PPI) were predicted using STRING and associations between hub gene and clinic features were analyzed using R software. The hub gene was silenced in HCC cell lines followed by cell behaviors analyses. A prognosis associated 14-gene model was identified in this study which could significantly distinguish samples into high-risk and low-risk groups. PBK, BUB1, NUF2, and CDCA8 were the key nodes involved in the 14 gene-coded PPI with high diagnostic values, and only PBK was an independent risk factor of disease specific survival (DSS) of HCC. Moreover, higher PBK was positively correlated with pathological and histological grades, higher AFP, and infiltrations of Th2, T helper cells and aDC of HCC, but negatively correlated with the killer immune cells. Dysregulated methylation might contribute to the higher expression of PBK and silencing PBK significantly suppressed the proliferation, growth, migration, and invasion of HCC cells. PBK, BUB1, NUF2, and CDCA8 played crucial role in prognosis associated 14-gene model with high diagnostic values. Methylation dysregulation-induced PBK accumulation might promote the development of HCC via modulating immune surveillance.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-024-10324-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761783","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
L6H21 stabilizing gut barrier improves EtOH-LPS-induced hepatic steatosis and injury in mice L6H21 稳定肠道屏障,改善 EtOH-LPS 诱导的小鼠肝脏脂肪变性和损伤
IF 2.9 4区 生物学
Journal of Molecular Histology Pub Date : 2025-04-03 DOI: 10.1007/s10735-025-10410-w
Li Ren, Xiaoxia Kong, Chen Mi, Fengyuan Li, Tuo Shao, Zhiming Hao
{"title":"L6H21 stabilizing gut barrier improves EtOH-LPS-induced hepatic steatosis and injury in mice","authors":"Li Ren,&nbsp;Xiaoxia Kong,&nbsp;Chen Mi,&nbsp;Fengyuan Li,&nbsp;Tuo Shao,&nbsp;Zhiming Hao","doi":"10.1007/s10735-025-10410-w","DOIUrl":"10.1007/s10735-025-10410-w","url":null,"abstract":"<div><p>This study aimed to investigate the role of (E)-2,3-dimethoxy-4′-methoxychalcone (L6H21) in alcoholic liver disease (ALD) by considering the connection among alcohol intake, gut microbiota-related intestinal endothelial barrier dysfunction, and ALD. Male C57BL/6J mice (8 weeks old) were randomly assigned to 8 experimental groups (<i>n</i> = 5/group), including those fed a control isocaloric liquid diet (Control), a Lieber-DeCarli liquid alcohol diet with 5% ethanol (EtOH group), and mice in the EtOH + LPS group or LPS group receiving LPS on Day 10. Other four groups (L6H21 group, LPS + L6H21 group, EtOH + L6H21 group, EtOH + LPS + L6H21 group) received L6H21 treatment at 10 mg/kg body weight/day via oral gavage starting from the experiment’s onset. Histological analysis (liver and ileum) and biochemical assays (serum and hepatic tissues) were performed in mice, while real-time PCR, Western blots, and immunofluorescence staining were used to investigate underlying mechanisms. In mice, EtOH-LPS induction led to significant increases in hepatic steatosis, hepatic inflammation, and serum ALT and AST levels. L6H21 treatment significantly reversed these changes. Furthermore, L6H21 treatment also reduced serum total cholesterol and hepatic triglyceride levels. In the intestine, L6H21 suppressed alcohol- and LPS-induced mucosal lesions and bacterial translocation, restored tight junction protein function, inhibited inflammation, and attenuated ROS production. L6H21 represents a promising therapeutic candidate for the intervention of ALD.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Evaluating TGF-β1 gene expression and promoter polymorphism in cervical cancer progression
IF 2.9 4区 生物学
Journal of Molecular Histology Pub Date : 2025-04-02 DOI: 10.1007/s10735-025-10402-w
Pavan Kumar Poleboyina, Akbar Pasha, S. K. Heena, Sneha Malleswari Poleboyina, Smita C. Pawar
{"title":"Evaluating TGF-β1 gene expression and promoter polymorphism in cervical cancer progression","authors":"Pavan Kumar Poleboyina,&nbsp;Akbar Pasha,&nbsp;S. K. Heena,&nbsp;Sneha Malleswari Poleboyina,&nbsp;Smita C. Pawar","doi":"10.1007/s10735-025-10402-w","DOIUrl":"10.1007/s10735-025-10402-w","url":null,"abstract":"<div><p>This study aims to investigate the TGF-β1 gene, which has significant prognostic value for early detection and diagnosis of cervical cancer, as well as TGF-β1 gene mRNA and protein expression and the association of promoter region (−509 C&gt;T) polymorphisms with cervical cancer (CC) development. Transcriptome analysis, immunohistochemistry, and RT-PCR were conducted to determine the gene expression of TGF-β1. The PCR-SSCP and Sanger sequencing methods were employed to test and validate the TGF-β1 −509C&gt;T promoter polymorphism in cervical squamous cell carcinoma in comparison to control samples. TGF-β1 is a cytokine that plays a role in tumorigenesis as well as physiological and pathological processes. It appeared as one of the most over-expressed genes identified through the clariom D transcriptome microarray, which describes its role in cancer progression. The results showed a significant TGF-β1 upregulation in CC compared to normal cervical tissue was confirmed using immunohistochemistry and real-time PCR. The levels of TGF-β1 were also determined using a receiver operating characteristic (ROC) curve to distinguish diseased from normal individuals. TGF-β1 ROC showed good selectivity in distinguishing malignant CC from non-malignant cervical tissues. The −509 C&gt;T promoter polymorphism in the TGF-β1 gene is found to be significantly more common in the disease group, and in-silico analysis (using the AliBaba2.0 gene regulation tool) confirms its correlation to the loss of myogenin transcription factor binding site, may resulting in TGF-β1 overexpression.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Blue light-emitting diode promotes mineralization of stem cells from the apical papilla via cryptochrome 1/Wnt/β-catenin signaling
IF 2.9 4区 生物学
Journal of Molecular Histology Pub Date : 2025-04-01 DOI: 10.1007/s10735-025-10400-y
Lin Ye, Hao Li, Wantong Zhang, Yan Zhou, Xiaorong Lan, Yao Wang
{"title":"Blue light-emitting diode promotes mineralization of stem cells from the apical papilla via cryptochrome 1/Wnt/β-catenin signaling","authors":"Lin Ye,&nbsp;Hao Li,&nbsp;Wantong Zhang,&nbsp;Yan Zhou,&nbsp;Xiaorong Lan,&nbsp;Yao Wang","doi":"10.1007/s10735-025-10400-y","DOIUrl":"10.1007/s10735-025-10400-y","url":null,"abstract":"<div><p>This study aimed to determine whether low-intensity blue LED light (4 J/cm<sup>2</sup>) promotes mineralization of stem cells from the apical papilla (SCAPs) by modulating <i>CRY1</i> expression and to elucidate the underlying molecular mechanisms. SCAPs identity was validated using flow cytometry. In a controlled experimental design, SCAPs were exposed to blue LED light, followed by quantitative assessment of <i>CRY1</i> and osteogenic markers (Runx2, OSX, DSPP, DMP-1) via qRT-PCR, Western blotting, and osteogenic staining. To investigate the role of <i>CRY1</i> in SCAPs osteogenic differentiation, <i>CRY1</i> was overexpressed using lentiviral transfection. Additionally, the Wnt/β-catenin pathway was analyzed using specific inhibitors (XAV-939) to elucidate the underlying molecular mechanisms. Blue LED irradiation reduced <i>CRY1</i> mRNA expression to 80% (day 7) and 45% (day 14) of control levels. <i>CRY1</i> overexpression significantly increased <i>CRY1</i> mRNA and protein levels (<i>P</i> &lt; 0.001) but decreased ALP activity and ARS staining (<i>P</i> &lt; 0.001). Blue LED treatment restored mineralization parameters to 80% of control levels. Key osteogenic genes (DMP-1, DSPP, Runx2, OSX) showed lower mRNA and protein levels in the <i>CRY1</i> overexpression group compared to controls. Blue LED exposure increased these levels to 60–74% (mRNA) and 45–67% (protein) of control values. In the Wnt/β-catenin pathway, <i>CRY1</i> overexpression elevated GSK-3β and reduced p-GSK-3β, β-catenin, and nuclear β-catenin levels. Blue LED treatment restored these levels to 33–54% of control values, indicating pathway activation. Inhibition of the Wnt/β-catenin pathway (using XAV-939) abolished differences in osteogenic gene expression and mineralization between <i>CRY1</i> overexpression and blue LED-treated groups, confirming its critical role. Blue LED light at 4 J/cm<sup>2</sup> enhances SCAPs mineralization by modulating <i>CRY1</i> expression and activating the Wnt/β-catenin pathway. These findings provide mechanistic insights into photobiomodulation (PBM) in bone regeneration and highlight its potential for tissue engineering and regenerative medicine.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143749210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Fatty acid binding protein 4 knockdown improves fetal development in rats with gestational diabetes mellitus through modulating autophagy mediated by the PTEN/Akt/mTOR signaling pathway
IF 2.9 4区 生物学
Journal of Molecular Histology Pub Date : 2025-03-29 DOI: 10.1007/s10735-025-10398-3
Fanglei Yang, Yifan Mao, Bin Tang, Rui Xu, Feiyun Jiang
{"title":"Fatty acid binding protein 4 knockdown improves fetal development in rats with gestational diabetes mellitus through modulating autophagy mediated by the PTEN/Akt/mTOR signaling pathway","authors":"Fanglei Yang,&nbsp;Yifan Mao,&nbsp;Bin Tang,&nbsp;Rui Xu,&nbsp;Feiyun Jiang","doi":"10.1007/s10735-025-10398-3","DOIUrl":"10.1007/s10735-025-10398-3","url":null,"abstract":"<div><p>We aimed to investigate whether fatty acid binding protein 4 (FABP4) knockdown can ameliorate fetal development in rats with gestational diabetes mellitus (GDM) through modulating autophagy mediated by the phosphatase and tensin homolog deleted on chromosome ten (PTEN)/serine/threonine protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway. Blank group (<i>n</i> = 12), GDM group (<i>n</i> = 12), small interfering negative control (si-NC) group (<i>n</i> = 12), si-FABP4 group (<i>n</i> = 12), and si-FABP4 + PTEN group (<i>n</i> = 12) were set up for the random assignment of pregnant rats. Compared to the blank group of pregnant rats, the serum FABP4 level, abortion rate, fasting insulin, homeostasis model assessment of insulin resistance index, development malformation rate and incidence rate of intrauterine growth restriction of fetal rats, as well as PTEN and Beclin-1 protein expressions and light chain 3 type II (LC3-ΙI)/LC3-Ι ratio in placental tissues rose significantly, while the phosphorylated (p)-Akt/Akt ratio, p62 protein expression, and p-mTOR/mTOR ratio in placental tissues dropped significantly in the GDM plus si-NC group (<i>P</i> &lt; 0.05). FABP4 knockdown improves fetal development in GDM rats, and its mechanism of action is probably related with the inhibited autophagy by regulating the PTEN/Akt/mTOR signaling pathway.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143735428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Temporospatial expression of neurogranin in the rat molar development
IF 2.9 4区 生物学
Journal of Molecular Histology Pub Date : 2025-03-29 DOI: 10.1007/s10735-025-10401-x
Jung-Sun Moon, Dong-Wook Yang, Dong-Hoo Kim, Jee-Hae Kang, Min-Seok Kim, Sun-Hun Kim
{"title":"Temporospatial expression of neurogranin in the rat molar development","authors":"Jung-Sun Moon,&nbsp;Dong-Wook Yang,&nbsp;Dong-Hoo Kim,&nbsp;Jee-Hae Kang,&nbsp;Min-Seok Kim,&nbsp;Sun-Hun Kim","doi":"10.1007/s10735-025-10401-x","DOIUrl":"10.1007/s10735-025-10401-x","url":null,"abstract":"<div><p>Differentiation and proliferation of odontogenic cells are regulated by specific genes, driving the morphological changes during tooth germ development. While substantial data have been gathered on genes involved in early tooth development, knowledge about the terminal differentiation of odontogenic cells—particularly ameloblasts—remains limited. To identify molecules involved in cytodifferentiation, gene expression profiles in maxillary cap stage and root stage molar germs of rats at postnatal day 9, respectively were compared using differential display-PCR. This analysis unexpectedly revealed the upregulation of neurogranin, a brain-specific calmodulin-binding protein, at the cap stage. The expression of neurogranin at both transcriptional and translational levels progressively decreased from the early bell stage, through the crown stage, to the root stage in molar germs. Similar temporal expression patterns were observed for other calmodulin-binding proteins, including neuromodulin and PEP-19. Immunofluorescence confirmed the presence of neurogranin in the inner enamel epithelium of cap and early bell stage molar germs. Correspondingly, the expression levels of calmodulin and PKCγ mRNA displayed dynamic changes during the developmental timeline. Notably, the ablation of neurogranin in SF2 ameloblastic cells enhanced ameloblast differentiation and mineralization. These findings, for the first time, suggest that neurogranin may play a critical role in the temporospatial regulation of the differentiation of inner enamel epithelial cells into ameloblasts.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143735429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
RING box protein-1 promotes the metastasis of cervical cancer through regulating matrix metalloproteinases via PI3K/AKT signaling pathway
IF 2.9 4区 生物学
Journal of Molecular Histology Pub Date : 2025-03-28 DOI: 10.1007/s10735-025-10396-5
Weiming Luo, Yunhai Li, Gang Li, Mei Yang
{"title":"RING box protein-1 promotes the metastasis of cervical cancer through regulating matrix metalloproteinases via PI3K/AKT signaling pathway","authors":"Weiming Luo,&nbsp;Yunhai Li,&nbsp;Gang Li,&nbsp;Mei Yang","doi":"10.1007/s10735-025-10396-5","DOIUrl":"10.1007/s10735-025-10396-5","url":null,"abstract":"<div><p>Cervical cancer (CC) remains a leading cause of cancer mortality amongst females worldwide. Some of the CC patients may experience early metastases of the primary tumor, however the underlying mechanism remains unclear. Aberrant expression of RING box protein-1 (RBX1), a subunit in the E3 ubiquitin ligase family, has been reported in several cancer types. Nevertheless, little is known regarding the role of RBX1 in the metastasis of CC patients. In this study, we examined the expression of RBX1 from 90 biopsies of CC patients, and found a significantly increased expression of RBX1 in the tumor tissues compared to the normal tissues. Notably, the abundance of RBX1 in the CC patients with metastasis was higher than their counterparts without metastasis, suggesting that RBX1 may play a significant role in the modulation of CC metastasis. Furthermore, by using Hela cells as a model of CC in vitro, we demonstrated that ectopic over-expression of RBX1 could significantly promote the migration and invasion of Hela cells, whereas knockdown of RBX1 could remarkably suppress the migration and invasion of Hela cells. Mechanistically, the regulatory effect of RBX1 on cell metastasis was associated with changes in matrix metalloproteinases (MMP3 and MMP9) and altered activity of PI3K/AKT signaling. In conclusion, this study highlighted RBX1 as a novel target that can promote the metastasis of Hela cells in vitro, which may contribute to the development of alternative therapeutic options for CC patients.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143716988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Localization and function of APC15 during mouse oocyte meiotic progression
IF 2.9 4区 生物学
Journal of Molecular Histology Pub Date : 2025-03-28 DOI: 10.1007/s10735-025-10404-8
Shi-Bin Chao, Ren-Ren Zhang, Qing-Yuan Sun
{"title":"Localization and function of APC15 during mouse oocyte meiotic progression","authors":"Shi-Bin Chao,&nbsp;Ren-Ren Zhang,&nbsp;Qing-Yuan Sun","doi":"10.1007/s10735-025-10404-8","DOIUrl":"10.1007/s10735-025-10404-8","url":null,"abstract":"<div><p>The Anaphase-Promoting Complex/Cyclosome (APC/C) is a critical regulator of cell cycle progression, with APC15 serving as an essential subunit. While the role of APC15 in mitosis is well characterized, its function during meiosis remains poorly understood. In this study, we investigated the expression, subcellular localization, and potential role of APC15 during mouse oocyte meiotic progression. Using immunofluorescence and confocal microscopy, we observed dynamic changes in APC15 localization throughout meiotic progression. Knockdown of APC15 via siRNA did not affect spindle organization, but led to meiotic arrest at metaphase I (MI) and impaired the removal of BUB3 from kinetochores, suggesting a disruption in Spindle Assembly Checkpoint (SAC) inactivation. Our results highlight the involvement of APC15 in the regulation of SAC and the transition from metaphase to anaphase in oocytes. These findings contribute to our understanding of APC15’s role in meiotic regulation and provide insights into its potential impact on maintaining chromosomal stability during oocyte maturation.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143716934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Efficacy of curcumin-selenium nanoemulsion in alleviating oxidative damage induced by aluminum chloride in a rat model of Alzheimer’s disease
IF 2.9 4区 生物学
Journal of Molecular Histology Pub Date : 2025-03-28 DOI: 10.1007/s10735-025-10406-6
Safaa M. Awad, Yasser A. Attia, Hassan ElSayed, Shams H. Abdelhafez, Akaber T. Keshta, Eman Rashad, Heba M. A. Khalil, Aziza T. Fathy
{"title":"Efficacy of curcumin-selenium nanoemulsion in alleviating oxidative damage induced by aluminum chloride in a rat model of Alzheimer’s disease","authors":"Safaa M. Awad,&nbsp;Yasser A. Attia,&nbsp;Hassan ElSayed,&nbsp;Shams H. Abdelhafez,&nbsp;Akaber T. Keshta,&nbsp;Eman Rashad,&nbsp;Heba M. A. Khalil,&nbsp;Aziza T. Fathy","doi":"10.1007/s10735-025-10406-6","DOIUrl":"10.1007/s10735-025-10406-6","url":null,"abstract":"<div><p>Alzheimer’s disease (AD) is a common neurological disorder primarily affecting older adults. A hallmark of this condition is the generation of reactive oxygen species (ROS), leading to increased oxidative stress and cellular damage. Treatment with a curcumin-selenium nanoemulsion has been shown to enhance behavioural performance and mitigate degenerative changes induced by aluminium chloride (AlCl<sub>3</sub>). This nanoemulsion also reduced the activity of acetylcholinesterase (AChE) and lowered levels of key proteins, including Aβ, p53, tau, nuclear factor erythroid 2-related factor 2 (Nrf2), and tumour necrosis factor-alpha (TNF-α). Additionally, it significantly decreased nitric oxide (NO) levels in the brain while enhancing the activity of catalase (CAT) and superoxide dismutase (SOD). The study highlights the antioxidant and anti-inflammatory properties of the curcumin-selenium nanoemulsion, suggesting its potential as a therapeutic option for alleviating AD induced by AlCl<sub>3</sub>. These results are further supported by improvements in the histological structure of the cortex and hippocampus, as well as enhanced immunohistochmical assessment of glial fibrillary acidic protein (GFAP). Cur- Se-nanoemulsion, the current drug delivery technology, may lower the amount of amyloid-β in AD rat brain and considerably ameliorate the memory deficit that improve therapy efficacy in AD lesions.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143716989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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