Lin Shu-Qian, Tian Nini, Yao Xiang, Pan Xing-Hua, Li Zi-An, Wang Qiang, Gao Jin, Zhao Xi-Long, Ruan Guang-Ping
The Basic Medical Laboratory of the 920th Hospital of the Joint Logistics Support Force of PLA, Kunming, Yunnan, China.
The Integrated Engineering Research Center of Cell Biological Medicine of State and Regions, Kunming, Yunnan, China.
Stem Cell Res Ther. 2025 May 30;16(1):267. doi: 10.1186/s13287-025-04406-2.
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.
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.
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.
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.
骨髓干细胞（BMSC）对趋化因子和炎性因子的调节能力在多种疾病中具有重要作用。延缓BMSC衰老并恢复衰老BMSC的功能非常重要。
制备并鉴定小鼠BMSC。建立BMSC的TCAB1基因干扰（Sh-TCAB1）、干扰对照（Sh-NC）、过表达（OE-TCAB1）和过表达对照（OE-NC）稳定细胞系，分析TCAB1表达与BMSC细胞衰老的关系。进行转录组高通量测序以进一步分析TCAB1在BMSC衰老中的作用机制。
流式细胞术检测显示BMSC表型正常，通过成骨脂肪分化染色鉴定培养的细胞为BMSC。TCAB1干扰和过表达稳定株的荧光转染效率均为90%，成功构建了干扰和过表达TCAB1基因的稳定株。TCAB1过表达抑制BMSC衰老，而TCAB1干扰则加速BMSC衰老。转录组测序结果表明，TCAB1可调节与BMSC代谢和细胞周期相关的信号通路，发挥抗BMSC衰老的作用。
转录组测序表明，TCAB1抑制BMSC衰老的机制与细胞周期和代谢过程有关，并通过调节关键因子Slc2a1和Egln3的表达发挥抗BMSC衰老功能。本研究通过分子水平证实了TCAB1的表达与BMSC衰老密切相关，为细胞衰老的临床治疗提供了新技术。
