International Journal of Biochemistry & Cell Biology最新文献

{"title":"Acalabrutinib alleviates metabolic dysfunction–associated steatotic liver disease by regulating bile acid metabolism","authors":"Yanbo Wang,&nbsp;Shiwei Chen,&nbsp;Bingjue Ye,&nbsp;Zhenggang Yang,&nbsp;Yanning Liu,&nbsp;Guohua Lou,&nbsp;Cheng Zhou,&nbsp;Min Zheng","doi":"10.1016/j.biocel.2025.106786","DOIUrl":"10.1016/j.biocel.2025.106786","url":null,"abstract":"<div><div>Metabolic dysfunction–associated steatotic liver disease (MASLD) is a global epidemic of chronic liver disease currently lacking effective treatment. Evaluating the therapeutic effects of existing drugs on MASLD is a time and cost-effective strategy. Bruton's tyrosine kinase (BTK) is an inflammatory signaling molecule playing an important role in the progression of MASLD. Aclabrutinib, a BTK inhibitor approved for treating mantle-cell lymphoma and chronic lymphocytic leukemia, has not been investigated for its potential to treat MASLD. This study examined the therapeutic effects and mechanisms of aclabrutinib on MASLD using a high-fat diet-induced mouse model. Results demonstrated significant alleviation of pathological parameters associated with MASLD upon administration of aclabrutinib. TSE PhenoMaster results revealed that aclabrutinib increased energy expenditure in mice. Furthermore, aclabrutinib upregulated the expression of genes associated with thermogenesis and lipolysis in adipose tissues. Additionally, it inhibited the transcription of genes related to lipid absorption in the small intestine and liver, while increasing the expression of hormone-sensitive lipase, hepatic nuclear factor 4 alpha and fibroblast growth factor 21 in the liver. Further analysis indicated that aclabrutinib promoted the alternative pathway of bile acid synthesis while restoring gut microbiota homeostasis. The altered bile acid profiles upregulated G protein-coupled bile acid receptor 1 expression in adipose tissues as well as vitamin D receptor expression in liver and small intestine. Our findings suggest that by regulating bile acid metabolism and gut microbiota, aclabrutinib may promote thermogenesis and lipolysis, thereby alleviating MASLD. This study provides novel insights into clinical applications targeting BTK for treating MASLD.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"185 ","pages":"Article 106786"},"PeriodicalIF":3.4,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143947136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Morin inhibits the progression of 5-fluorouracil–resistant colorectal cancer by suppressing autophagy","authors":"Rui Li ,&nbsp;Fengxia Wang ,&nbsp;Lu Huang ,&nbsp;Lvheng Zhao ,&nbsp;Ting Qin ,&nbsp;Shan Liu ,&nbsp;Kunyao Xu ,&nbsp;Bi Wang ,&nbsp;Ling Li ,&nbsp;Sha He","doi":"10.1016/j.biocel.2025.106783","DOIUrl":"10.1016/j.biocel.2025.106783","url":null,"abstract":"<div><h3>Background</h3><div>Resistance to 5-fluorouracil (5-FU) poses a significant challenge in colorectal cancer (CRC) treatment. Morin is a flavonoid with anti-tumor properties. However, its role in overcoming acquired 5-FU resistance in CRC remains unclear.</div></div><div><h3>Methods</h3><div>5-FU-resistant CRC (5-FU/CRC) cell lines (HT29/5-FU and HCT116/5-FU) were established using the IC50 concentration increment method. After treatment with Morin and autophagy inhibitors (3-MA) or agonists (RAPA), cell viability, apoptosis, colony formation, migration, invasion, and autophagy were evaluated. <em>In vivo</em>, xenograft models of 5-FU/CRC assessed Morin's therapeutic effects.</div></div><div><h3>Results</h3><div>5-FU/CRC cells were successfully constructed. Morin inhibited the viability, migration, and invasion of 5-FU/CRC cells and promoted apoptosis. Morin also inhibited autophagy in 5-FU/CRC cells. Besides, autophagy activated by RAPA could eliminate the effect of Morin on 5-FU/CRC cells, while 3-MA enhanced the effects of Morin. In nude mouse models, Morin inhibited the growth and improved the pathological structure of 5-FU/CRC xenografts by inhibiting autophagy.</div></div><div><h3>Conclusion</h3><div>Morin suppresses the progression of 5-FU/CRC by inhibiting autophagy, suggesting its potential as a therapeutic agent to combat 5-FU resistance.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"185 ","pages":"Article 106783"},"PeriodicalIF":3.4,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143940976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of M2 macrophage-mediated mesenchymal stem cell migration: Boldine attenuates elbow heterotopic ossification","authors":"Fengteng Shen ,&nbsp;Yansong Chen ,&nbsp;Zhikun Xu ,&nbsp;Wei Wang ,&nbsp;Guofang Chen ,&nbsp;Fusheng Ye","doi":"10.1016/j.biocel.2025.106787","DOIUrl":"10.1016/j.biocel.2025.106787","url":null,"abstract":"<div><h3>Background</h3><div>Heterotopic ossification (HO) is characterized by abnormal bone formation in soft tissues, often following trauma or surgery. Transforming growth factor-beta (TGF-β) signaling and M2 macrophage polarization play critical roles in the recruitment and differentiation of mesenchymal stromal/progenitor cells (MSPCs), promoting HO.</div></div><div><h3>Methods</h3><div>An elbow joint trauma-induced HO mouse model was established, where model mice were treated with dichloromethylene-bisphosphonate (Cl2MBP) liposomes or PBS liposomes to deplete macrophages. In addition, boldine was administered to evaluate its therapeutic effect on HO formation. Bone marrow mesenchymal stem cells (BMSCs) were also extracted for <em>in vitro</em> experiments. Quantitative real-time PCR (qRT-PCR) and Western blot were conducted to assess gene and protein expression. <em>In vivo</em> methods included Micro-Computed Tomography (Micro-CT) to assess bone formation, histological staining to evaluate tissue changes, immunohistochemistry (IHC) and immunofluorescence to analyze macrophage, CD73⁺ and CD105⁺ cells infiltration. <em>In vitro</em>, BMSCs were identified by flow cytometry and treated with interleukin-10 (IL-10) and/or boldine, and assays such as cell viability (Cell Counting Kit 8 (CCK8)), migration (Transwell), immunofluorescence, ALP staining, and Alizarin Red S staining, were conducted to assess osteogenic differentiation.</div></div><div><h3>Results</h3><div>Boldine treatment significantly reduced HO formation, decreased collagen deposition, and inhibited M2 macrophage infiltration (<em>P</em> &lt; 0.05). <em>In vitro</em>, boldine reduced IL-10-induced cell activity, migration, and osteogenic differentiation of BMSCs and inhibited TGF-β and pSmad2/3/Smad2/3 protein (<em>P</em> &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>Boldine attenuates HO by inhibiting M2 macrophage-mediated MSPC migration and might involve the TGF-β signaling, suggesting its potential as a therapeutic approach for managing HO.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"185 ","pages":"Article 106787"},"PeriodicalIF":3.4,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143886988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of long non-coding RNA in lipid metabolism: Implications in leukemia","authors":"Anjani Alluri ,&nbsp;Pallavi Saxena ,&nbsp;Amit Mishra ,&nbsp;Ravi Kumar Gutti","doi":"10.1016/j.biocel.2025.106785","DOIUrl":"10.1016/j.biocel.2025.106785","url":null,"abstract":"<div><div>Cancer has high mortality rate and occupies second position among major diseases. Despite extensive research and therapies, in every nook and corner of the world, death rate is increasing exponentially. Hallmarks of cancer are benchmarks of cancer cells describing the fundamental principle and capabilities of the cells transforming from normal to malignant tumour. One of the major ones among them is the deregulation of cellular metabolism or metabolic reprogramming, involving alterations in glucose and lipid metabolism. Progressive research in this area has visualized the vital role of lncRNAs in lipid metabolism with respect to AML. lncRNAs involve in various cellular processes and also contribute for significant functions of the cell like chromatin remodelling, transcriptional activation and repression, gene regulation, immune response, cell differentiation, and cell cycle regulation, in addition to oncogenic processes such as proliferation, angiogenesis, migration, and apoptosis. Structural similarities are observed among mRNAs and lncRNAs in terms of poly A-tail and 5^’ cap however protein-coding regions are lacking. A large body of evidence has shown that lncRNAs directly or indirectly mediate lipid metabolism by activating downstream genes. Considering their potential involvement in leukemia, these lncRNAs can be explored and considered as biomarkers for therapeutics, prognosis, and diagnosis. The present review is planned to summarize the functional classification of lncRNAs, the role of lipid metabolism in cancer, different lncRNAs involved in leukemia, and different cancer types related to lipid metabolism.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"184 ","pages":"Article 106785"},"PeriodicalIF":3.4,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143848436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CAPRIN1/TYMS/MTHFD2 axis promotes EMT process in nasopharyngeal carcinoma development","authors":"Kunrong Wang ,&nbsp;Hanbing Yu ,&nbsp;Shuang Guo ,&nbsp;Guihu Sun ,&nbsp;Hongwei Cao ,&nbsp;Dongsheng Xing ,&nbsp;Dawei Li ,&nbsp;Aihui Yan","doi":"10.1016/j.biocel.2025.106784","DOIUrl":"10.1016/j.biocel.2025.106784","url":null,"abstract":"<div><h3>Background</h3><div>Nasopharyngeal carcinoma (NPC) is a type of malignant tumor occurring in the nasopharynx. It frequently leads to treatment failure after metastasis, often resulting from epithelial-mesenchymal transition (EMT). Thymidylate synthetase (TYMS) is a key enzyme involved in DNA synthesis and replication. Currently, the role of TYMS and its mechanism of upstream and downstream in EMT of NPC is unclear.</div></div><div><h3>Methods</h3><div>NPC cell lines HK-1 and C666–1 were used in this study. Lentivirus carrying TYMS knockdown and overexpressed plasmids were used to regulate TYMS expression. Cell migration and invasion were examined using the wound-healing and Transwell assays, respectively. C666–1 cells were injected into the axilla and tail vein of mice to form subcutaneous tumors and construct lung metastasis model, respectively. RNA immunoprecipitation assay was used to examine the interaction between protein and mRNA. RNA-seq was performed to explore the downstream regulatory mechanism of TYMS.</div></div><div><h3>Results</h3><div>TYMS was highly expressed in NPC tissues. TYMS silencing and upregulation inhibited and promoted EMT processes in NPC cells, respectively, as demonstrated by the expression of EMT-related proteins, including E-cadherin, Slug, MMP2, and MMP9. Cytoplasmic activation/proliferation-associated protein-1 (CAPRIN1), a protein bound with TYMS mRNA, promoted the EMT process in NPC cells. Meanwhile, TYMS knockdown reversed the effect of CAPRIN1 overexpression. Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) was down-regulated following TYMS silencing. MTHFD2 knockdown abolished the effect of TYMS overexpression.</div></div><div><h3>Conclusion</h3><div>CAPRIN1/TYMS/MTHFD2 axis drives the EMT process and thus promotes NPC development, which is a promising target in therapy and adjuvant therapy of NPC.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"185 ","pages":"Article 106784"},"PeriodicalIF":3.4,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143859721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-channel smFRET study reveals a compact conformation of EF-G on the ribosome","authors":"Jordan L. Johnson ,&nbsp;Jacob H. Steele ,&nbsp;Ran Lin ,&nbsp;Victor G. Stepanov,&nbsp;Miriam N. Gavriliuc ,&nbsp;Yuhong Wang","doi":"10.1016/j.biocel.2025.106782","DOIUrl":"10.1016/j.biocel.2025.106782","url":null,"abstract":"<div><div>While elongation factor G (EF-G) is crucial for ribosome translocation, the role of its GTP hydrolysis remains ambiguous. EF-G's indispensability is further exemplified by the phosphorylation of human eukaryotic elongation factor 2 (eEF2) at Thr56, which inhibits protein synthesis globally, but its exact mechanism is not clear. In this study, we developed a multi-channel single-molecule FRET (smFRET) microscopy methodology to examine the conformational changes of <em>E. coli</em> EF-G induced by mutations that closely aligned with eEF2's Thr56 residue. We utilized Alexa 488/594 double-labeled EF-G to catalyze the translocation of fMet-Phe-tRNA^Phe-Cy3 inside Cy5-L27 labeled ribosomes, allowing us to probe both processes within the same complex. Our findings indicate that in the presence of either GTP or GDPCP, wild-type EF-G undergoes a conformational extension upon binding to the ribosome to promote normal translocation. On the other hand, the T48E and T48V mutations did not affect GTP/GDP binding or GTP hydrolysis, but impeded Poly(Phe) synthesis and caused EF-G to adopt a unique compact conformation, which was not observed when the mutants interact solely with the SRL. This study provides new insights into EF-G's adaptability and sheds light on the modification mechanism of human eEF2.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"184 ","pages":"Article 106782"},"PeriodicalIF":3.4,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143816004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hematopoietic stem cell conditioned media induces apoptosis in colorectal cancer stem cells via dysregulation of HSP90 and 26S proteasome system","authors":"Sumit Mallick ,&nbsp;Vanya Kadla Narayana ,&nbsp;Akhila Balakrishna Rai ,&nbsp;Shubham Sukerndeo Upadhyay ,&nbsp;Thottethodi Subrahmanya Keshava Prasad ,&nbsp;Sudheer Shenoy P ,&nbsp;Bipasha Bose (Lead contact)","doi":"10.1016/j.biocel.2025.106773","DOIUrl":"10.1016/j.biocel.2025.106773","url":null,"abstract":"<div><div>Cancer stem cells (CSCs) hold a significant role in cancer metastasis, high mortality and severity responsible for therapy resistance and tumour recurrence. The 26S proteasome system plays a major role in protein degradation in normal cells. As most cancers have upregulated 26S proteasome machinery, cancer cells use the 26S proteasome system in their favour for growth support by degrading unwanted proteins, but dysfunction of the 26S proteasome system induces apoptosis in cells. Here, we used hematopoietic stem cells (HSCs) and HSCs-derived conditioned media (CM) to target colorectal cancer stem cells (CRC-CSCs). HSCs are otherwise used extensively to save the lives of patients suffering from hematological malignancies and inherited blood disorders. HSCs-derived conditioned media contains various cytokines, chemokines, and secretory small molecules, which can also target the CRC-CSCs. Moreover, HSCs have exhibited CRC-CSC tropism in vitro in our pilot studies. As therapeutic uses of HSCs for targeting colorectal cancer (CRC) have never been reported, we hypothesized the CRC-CSC targeting properties of HSCs. Our results indicated altered protein function of CRC-CSCs upon co-culture with HSCs. Proteomics approaches showed that HSCs-CM disrupted 26S proteasomal complex and altered the mitochondrial bioenergetics, thereby activating apoptosis in CRC-CSCs. Furthermore, we observed that HSCs-CM significantly induced double-stranded DNA damage and proteasomal degradation, leading to apoptosis and upregulating the autophagy system. This study, hence, provides the prospective targeting of cancer stem cells using HSCs-CM, indicating a possible therapeutic approach.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"184 ","pages":"Article 106773"},"PeriodicalIF":3.4,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143842684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial and peroxisomal fission in cortical neurogenesis","authors":"Gabriella L. Robertson ,&nbsp;Caroline Bodnya ,&nbsp;Vivian Gama","doi":"10.1016/j.biocel.2025.106774","DOIUrl":"10.1016/j.biocel.2025.106774","url":null,"abstract":"<div><div>The human brain is unique in its cellular diversity, intricate cytoarchitecture, function, and complex metabolic and bioenergetic demands, for which mitochondria and peroxisomes are essential. Mitochondria are multifunctional organelles that coordinate various signaling pathways central to neurogenesis. The dynamic morphological changes of the mitochondrial network have been linked to the regulation of bioenergetic and metabolic states. Specific protein machinery is dedicated to mitochondrial fission and fusion, allowing organelle distribution during cell division, organelle repair, and adaptation to environmental stimuli (excellent reviews have been published on these topics [<span><span>Kondadi and Reichert, 2024</span></span>; <span><span>Giacomello et al., 2020</span></span>; <span><span>Tilokani et al., 2018</span></span>; <span><span>Kraus et al., 2021</span></span>; <span><span>Navaratnarajah et al., 2021</span></span>]). In parallel, peroxisomes contain over 50 different enzymes which regulate metabolic functions that are critical for neurogenesis (<span><span>Berger et al., 2016</span></span>, <span><span>Hulshagen et al., 2008</span></span>). Peroxisomes share many of the components of their fission machinery with the mitochondria and undergo fission to help meet metabolic demands in response to environmental stimuli (<span><span>Schrader et al., 2016</span></span>). This review focuses primarily on the machinery involved in mitochondrial and peroxisomal fission. Mitochondrial fission has been identified as a critical determinant of cell fate decisions (<span><span>Iwata et al., 2023</span></span>, <span><span>Iwata et al., 2020</span></span>, <span><span>Khacho et al., 2016</span></span>, <span><span>King et al., 2021</span></span>, <span><span>Prigione and Adjaye, 2010</span></span>, <span><span>Vantaggiato et al., 2019</span></span>, <span><span>Kraus et al., 2021</span></span>). The connection between alterations in peroxisomal fission and metabolic changes associated with cellular differentiation remains less clear. Here, we provide an overview of the functional and regulatory aspects of the mitochondrial and peroxisomal fission machinery and provide insight into the current mechanistic understanding by which mitochondrial and peroxisomal fission influence neurogenesis.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"182 ","pages":"Article 106774"},"PeriodicalIF":3.4,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143755855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selective cerebral hypothermia alleviates focal cerebral ischemia/reperfusion injury via enhancing SUMO2/3 modification of Drp1 in rats","authors":"Yang Yuan ,&nbsp;Li Fu ,&nbsp;Wenji Liu ,&nbsp;Rui Dong ,&nbsp;Fei Shi ,&nbsp;Jinhao Liu ,&nbsp;Hong Li ,&nbsp;Gaofeng Zhang","doi":"10.1016/j.biocel.2025.106772","DOIUrl":"10.1016/j.biocel.2025.106772","url":null,"abstract":"<div><h3>Background</h3><div>Selective Cerebral Hypothermia (SCH) has been demonstrated to potentiate SUMO2/3 modification, a native cellular safeguard against Cerebral Ischemia/Reperfusion Injury (CIRI). Dynamin-Related Protein 1 (Drp1), a pivotal regulator in the mitochondrial fission pathway, is an important substrate for SUMO2/3 modification. However, effects of SCH on SUMO2/3 modification of Drp1 remain undefined. Herein, the current study posits that SCH augments the SUMO2/3 modification of Drp1, thereby preserving mitochondrial integrity and mitigating CIRI.</div></div><div><h3>Methods</h3><div>A focal CIRI model was established in Sprague-Dawley rats, with 20°C saline perfused via the transcarotid artery to induce SCH condition, and 37°C saline serving as a control. The modified Neurological Severity Score (mNSS) was used to quantitate the degree of neurological deficits. Staining of 2,3–5-triphenyltetrazolium chloride (TTC) was performed to detect cerebral infarction volume. Histological change of neurocyte was observed through Hematoxylin-eosin (HE) staining. Neurocyte apoptosis was evaluated using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) immunofluorescence staining. Western blot (WB) was utilized to evaluated the expressions of Drp1 and Cytochrome C. Co-immunoprecipitation was performed to evaluate the level of SUMO2/3 modification of Drp1. And transmission electron microscopy was used to observe the mitochondrial ultrastructure. The ratio of M-Drp1 to T-Drp1 and mitochondria morphological changes were observed under confocal microscopy.</div></div><div><h3>Results</h3><div>Research data revealed that SCH significantly enhanced the SUMO2/3 modification of Drp1 when CIRI occurred. Concurrently, mNSSs, cerebral infarct volume, and apoptotic rates were notably attenuated in the SCH group, corroborating SCH's protective role. Expression levels of mitochondrial outer membrane Drp1 (M-Drp1), cytoplasmic cytochrome C (C-CytC), and ratio of M-Drp1 to T-Drp1 were reduced, and changes of mitochondrial ultrastructural and morphology were mitigated, underscoring SCH's inhibitory effect on mitochondrial fission. In contrast, 37°C saline displayed negligible protective impact while compare with 20°C saline perfusion.</div></div><div><h3>Conclusions</h3><div>The findings support that SCH amplifies SUMO2/3 modification of Drp1, curtails excessive mitochondrial fission, and consequently ameliorates focal CIRI in a rat model.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"182 ","pages":"Article 106772"},"PeriodicalIF":3.4,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143681915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory role of TEX10 gene in proliferation differentiation and apoptosis of bovine myoblasts","authors":"Yongpan Wang ,&nbsp;Zijing Zhang ,&nbsp;Yuqiao Zhang ,&nbsp;Jiamei Wang ,&nbsp;Shijie Lyu ,&nbsp;Xian Liu ,&nbsp;Xingshan Qi ,&nbsp;Weidong Ma ,&nbsp;Chuzhao Lei ,&nbsp;Eryao Wang ,&nbsp;Yongzhen Huang","doi":"10.1016/j.biocel.2025.106771","DOIUrl":"10.1016/j.biocel.2025.106771","url":null,"abstract":"<div><div>Skeletal muscle is a crucial tissue involved in body movement and energy metabolism, and its growth and development directly influence the economic value of livestock. This study investigates the effects of the <em>TEX10</em> gene on the proliferation, differentiation, and apoptosis of bovine myoblasts, as well as the underlying molecular mechanisms. Using techniques such as CCK-8, EdU incorporation, qPCR, Western blotting, and immunofluorescence, we observed that <em>TEX10</em> significantly promotes the expression of cell cycle factors, including <em>CDK2</em> and <em>PCNA</em>, thereby increasing cell proliferation and the proportion of cells in the S phase. Overexpression and knockdown experiments demonstrated that <em>TEX10</em> enhances the differentiation and myotube formation of myoblasts, while upregulating key genes such as <em>MYOG</em> and <em>MYOD</em>. Additionally, flow cytometry analysis of the cell cycle revealed that <em>TEX10</em> inhibits apoptosis in bovine myoblasts. Transcriptomic analysis showed that <em>TEX10</em> regulates several signaling pathways associated with proliferation, differentiation, and apoptosis, including PI3K-Akt, cAMP, and IL-17. Overall, these findings suggest that <em>TEX10</em> plays a significant regulatory role in bovine muscle growth, providing a theoretical foundation for molecular breeding strategies aimed at improving yellow cattle.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"182 ","pages":"Article 106771"},"PeriodicalIF":3.4,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}