间充质干细胞
基因剔除小鼠
条件基因敲除
骨髓
干细胞
细胞生物学
脂肪生成
化学
生物
免疫学
表型
受体
生物化学
基因
作者
Qiannan Niu,Shuning Shen,Jiaojiao He,Lei Wang
出处
期刊:Regenerative Medicine
[Future Medicine]
日期:2021-09-01
卷期号:16 (9): 847-859
被引量:3
标识
DOI:10.2217/rme-2020-0119
摘要
Background: Osteogenesis greatly depends on the differentiation of bone marrow mesenchymal stem cells (BMSCs). CKIP-1 is considered to be a negative regulator of BMSCs. Methods: We established a CKIP-1 knockout mouse model, then isolated and cultured BMSCs from wild-type and knockout groups. Results: Our data demonstrated that CKIP-1 knockout significantly increased bone structure in the experimental mouse model and enhanced BMSC proliferation. CKIP-1 knockout contributed to osteoblastic and adipogenic differentiation. Furthermore, CKIP-1 regulated osteogenesis in BMSCs via the MAPK signaling pathway, and BMSCs from the CKIP-1 knockout mice were effective in repairing the skull defect null mice. Conclusion: Our results concluded that silencing of CKIP-1 promoted osteogenesis in experimental mice and increased BMSCs differentiation via upregulation of the MAPK signaling pathway.
科研通智能强力驱动
Strongly Powered by AbleSci AI