分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

LncAABR07053481 inhibits bone marrow mesenchymal stem cell apoptosis and promotes repair following steroid-induced avascular necrosis

Wang Tao, Xie Zhi-Hong, Wang Lei, Luo Hong, Zhang Jian, Dong Wen-Tao, Zheng Xiao-Han, Ye Chuan, Tian Xiao-Bin, Liu Gang, Zhu Xue-Song, Li Yan-Lin, Kang Qing-Lin, Zhang Fei, Peng Wu-Xun

Journal:Communications Biology

IF:5.9

DOI:10.1038/s42003-023-04661-0

PMID:37012358

Published:2023-04-03

research field:分子生物学干细胞生物学再生医学骨科

Abstract

The osteonecrotic area of steroid-induced avascular necrosis of the femoral head (SANFH) is a hypoxic microenvironment that leads to apoptosis of transplanted bone marrow mesenchymal stem cells (BMSCs). However, the underlying mechanism remains unclear. Here, we explore the mechanism of hypoxic-induced apoptosis of BMSCs, and use the mechanism to improve the transplantation efficacy of BMSCs. Our results show that the long non-coding RNA AABR07053481 (LncAABR07053481) is downregulated in BMSCs and closely related to the degree of hypoxia. Overexpression of LncAABR07053481 could increase the survival rate of BMSCs. Further exploration of the downstream target gene indicates that LncAABR07053481 acts as a molecular “sponge” of miR-664-2-5p to relieve the silencing effect of miR-664-2-5p on the target gene Notch1 . Importantly, the survival rate of BMSCs overexpressing LncAABR07053481 is significantly improved after transplantation, and the repair effect of BMSCs in the osteonecrotic area is also improved. This study reveal the mechanism by which LncAABR07053481 inhibits hypoxia-induced apoptosis of BMSCs by regulating the miR-664-2-5p/ Notch1 pathway and its therapeutic effect on SANFH.

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