miR-203-3p promotes senescence of mouse bone marrow mesenchymal stem cells via downregulation of Pbk.

Qiaojuan Mei, Kexin Li, Tianyu Tang, Siying Cai, Yu Liu, Xiaofei Wang, Yinzhao Jia, Ling Zhang, Huaibiao Li, Hui Song, Jun Zhai, Wenpei Xiang

Institute of Reproductive Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. · pubmed

Paper

Abstract

The senescence of bone marrow mesenchymal stem cells (BMSCs) contributes to the development of degenerative skeletal conditions. To date, the molecular mechanism resulting in BMSC senescence has not been fully understood. In this study, we identified a small non-coding RNA, miR-203-3p, the expression of which was elevated in BMSCs from aged mice. On the other hand, overexpression of miR-203-3p in BMSCs from young mice reduced cell growth and enhanced their senescence. Mechanistically, PDZ-linked kinase (PBK) is predicted to be the target of miR-203-3p. The binding of miR-203-3p to Pbk mRNA could decrease its expression, which in turn inhibited the ubiquitination-mediated degradation of p53. Furthermore, the intravitreal injection of miR-203-3p-inhibitor into the bone marrow cavity of aged mice attenuated BMSC senescence and osteoporosis in aged mice. Collectively, these findings suggest that targeting miR-203-3p to delay BMSC senescence could be a potential therapeutic strategy to alleviate age-related osteoporosis.

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Research summary

The paper investigates the role of miR-203-3p in promoting senescence of bone marrow mesenchymal stem cells, which is directly related to the aging process and age-related conditions like osteoporosis. While it provides insights into a potential therapeutic target for delaying BMSC senescence, the findings are incremental and primarily focus on a specific mechanism rather than addressing broader aspects of aging or lifespan extension. Thus, while relevant, the impact is limited.

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