Regulation of base excision repair during adipogenesis and osteogenesis of bone marrow-derived mesenchymal stem cells

被引:2
|
作者
Kim, Min [1 ]
Jang, Hyun-Jin [1 ]
Baek, Song-Yi [1 ]
Choi, Kyung-Jin [1 ]
Han, Dong-Hee [1 ]
Sung, Jung-Suk [1 ]
机构
[1] Dongguk Univ Seoul, Dept Life Sci, Biomed Campus,32 Dongguk Ro, Goyang 10326, Gyeonggi Do, South Korea
基金
新加坡国家研究基金会;
关键词
DNA-POLYMERASE-BETA; DAMAGE REPAIR; DIFFERENTIATION; EXPRESSION; CANCER; XRCC1; COORDINATION; GLYCOSYLASES; PROTECTION; DECREASES;
D O I
10.1038/s41598-023-43737-z
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Bone marrow-derived human mesenchymal stem cells (hMSCs) can differentiate into various lineages, such as chondrocytes, adipocytes, osteoblasts, and neuronal lineages. It has been shown that the high-efficiency DNA-repair capacity of hMSCs is decreased during their differentiation. However, the underlying its mechanism during adipogenesis and osteogenesis is unknown. Herein, we investigated how alkyl-damage repair is modulated during adipogenic and osteogenic differentiation, especially focusing on the base excision repair (BER) pathway. Response to an alkylation agent was assessed via quantification of the double-strand break (DSB) foci and activities of BER-related enzymes during differentiation in hMSCs. Adipocytes showed high resistance against methyl methanesulfonate (MMS)-induced alkyl damage, whereas osteoblasts were more sensitive than hMSCs. During the differentiation, activities, and protein levels of uracil-DNA glycosylase were found to be regulated. In addition, ligation-related proteins, such as X-ray repair cross-complementing protein 1 (XRCC1) and DNA polymerase beta, were upregulated in adipocytes, whereas their levels and recruitment declined during osteogenesis. These modulations of BER enzyme activity during differentiation influenced DNA repair efficiency and the accumulation of DSBs as repair intermediates in the nucleus. Taken together, we suggest that BER enzymatic activity is regulated in adipogenic and osteogenic differentiation and these alterations in the BER pathway led to different responses to alkyl damage from those in hMSCs.
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页数:13
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