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Updated: May 21, 2026

Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
Sec31a and its impact on ER stress and Bmp/Smad signaling in senescent BMSCs
Jiaming Nie1, Tuohutibu Abukelimu1, Jingzhi Ma1
1Department of Stomatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Abstract:
Cellular senescence diminishes the osteogenic potential of bone marrow mesenchymal stem cells (BMSCs), leading to age-related maxillofacial bone loss. As a key element of COPII vesicles, Sec31a is essential for endoplasmic reticulum (ER)-to-Golgi transport. Nevertheless, the impact of Sec31a on BMSCs senescence needs further investigation. Our research revealed a remarkable reduction of Sec31a levels in D-galactose (D-gal)-induced senescent BMSCs, concurrent with elevated ER stress and diminished osteogenic differentiation. Knockdown of Sec31a further intensified ER stress, suppressed Bmp4/Smad signaling, and further impaired osteogenesis in senescent BMSCs. Therefore, Sec31a modulates osteogenic differentiation in aged BMSCs through the Bmp4/Smad signaling pathway and via ER stress through a mechanism independent of this pathway. Our findings provide a theoretical perspective for treating age-related maxillofacial bone defects.
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