{"title":"The mechanism of telomerase Cajal body protein 1 regulating senescence of mouse bone marrow mesenchymal stem cells.","authors":"Shu-Qian Lin, Nini Tian, Xiang Yao, Xing-Hua Pan, Zi-An Li, Qiang Wang, Jin Gao, Xi-Long Zhao, Guang-Ping Ruan","doi":"10.1186/s13287-025-04406-2","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>The regulatory ability of bone marrow stem cells (BMSC) to chemokines and inflammatory factors has a significant effect in a variety of diseases. It is very important to delay the aging of BMSC and restore the function of aging BMSC.</p><p><strong>Methods: </strong>Mouse BMSC was prepared and identified. TCAB1 gene interference (Sh-TCAB1), interference control (Sh-NC), overexpression (OE-TCAB1) and overexpression control (OE-NC) stable cell lines of BMSC were established, and the relationship between TCAB1 expression and senescence of BMSC cells was analyzed. Transcriptome high-throughput sequencing was performed to further analyze the mechanism of TCAB1 in BMSC aging.</p><p><strong>Results: </strong>The phenotype of BMSC was normal by flow cytometry, and the cultured cells were identified as BMSC by osteogenic lipogenic differentiation staining. The fluorescence transfection efficiency of TCAB1-interfered and overexpressed stable strain was 90%, and the stable strain of interfered and overexpressed TCAB1 gene was successfully constructed. Overexpression of TCAB1 inhibits BMSC senescence, and TCAB1 interferes with and accelerates BMSC senescence. Transcriptome sequencing results show that TCAB1 can regulate signaling pathways related to BMSC metabolism and cell cycle to play an anti-BMSC senescence role.</p><p><strong>Conclusion: </strong>Transcriptome sequencing suggests that the mechanism of TCAB1 inhibiting BMSC senescence is related to cell cycle and metabolic process, and exerts anti-BMSC senescence function by regulating the expression of key factors Slc2a1 and Egln3. This study confirmed that the expression of TCAB1 is closely related to the senescence of BMSC through molecular level, which provides a new technique for the clinical treatment of cell senescence.</p>","PeriodicalId":21876,"journal":{"name":"Stem Cell Research & Therapy","volume":"16 1","pages":"267"},"PeriodicalIF":7.1000,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12123861/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Stem Cell Research & Therapy","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s13287-025-04406-2","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CELL & TISSUE ENGINEERING","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: The regulatory ability of bone marrow stem cells (BMSC) to chemokines and inflammatory factors has a significant effect in a variety of diseases. It is very important to delay the aging of BMSC and restore the function of aging BMSC.
Methods: Mouse BMSC was prepared and identified. TCAB1 gene interference (Sh-TCAB1), interference control (Sh-NC), overexpression (OE-TCAB1) and overexpression control (OE-NC) stable cell lines of BMSC were established, and the relationship between TCAB1 expression and senescence of BMSC cells was analyzed. Transcriptome high-throughput sequencing was performed to further analyze the mechanism of TCAB1 in BMSC aging.
Results: The phenotype of BMSC was normal by flow cytometry, and the cultured cells were identified as BMSC by osteogenic lipogenic differentiation staining. The fluorescence transfection efficiency of TCAB1-interfered and overexpressed stable strain was 90%, and the stable strain of interfered and overexpressed TCAB1 gene was successfully constructed. Overexpression of TCAB1 inhibits BMSC senescence, and TCAB1 interferes with and accelerates BMSC senescence. Transcriptome sequencing results show that TCAB1 can regulate signaling pathways related to BMSC metabolism and cell cycle to play an anti-BMSC senescence role.
Conclusion: Transcriptome sequencing suggests that the mechanism of TCAB1 inhibiting BMSC senescence is related to cell cycle and metabolic process, and exerts anti-BMSC senescence function by regulating the expression of key factors Slc2a1 and Egln3. This study confirmed that the expression of TCAB1 is closely related to the senescence of BMSC through molecular level, which provides a new technique for the clinical treatment of cell senescence.
期刊介绍：
Stem Cell Research & Therapy serves as a leading platform for translational research in stem cell therapies. This international, peer-reviewed journal publishes high-quality open-access research articles, with a focus on basic, translational, and clinical research in stem cell therapeutics and regenerative therapies. Coverage includes animal models and clinical trials. Additionally, the journal offers reviews, viewpoints, commentaries, and reports.
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