Suppr超能文献

KLF9 调节间充质干细胞的成骨分化。

KLF9 regulates osteogenic differentiation of mesenchymal stem cells.

机构信息

The State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.

Faculty of Chinese Medicine, Hunan Traditional Chinese Medical College, Zhuzhou, China.

出版信息

J Mol Histol. 2024 Aug;55(4):503-512. doi: 10.1007/s10735-024-10204-6. Epub 2024 May 27.

Abstract

Osteoporosis is a progressive skeletal disease which is characterized by reduced bone mass and degradation of bone microstructure. Mesenchymal stem cells (MSCs) have the potential to inhibit osteoporosis since they are multipotent stem cells that can differentiate into multiple types of cells including osteoblasts. Hence the mechanism of osteogenic differentiation of MSCs deserves comprehensive study. Here we report that KLF9 is a novel regulator in osteogenic differentiation of MSCs. We observed that depletion of KLF9 can largely compromise the osteogenic differentiation ability of MSCs. In addition, we revealed that inhibition of the PI3K-Akt pathway could also affect osteogenic differentiation since KLF9 depletion inhibits PI3K expression. Finally, we discovered that KLF9 expression can be induced by dexamethasone which is an essential component in osteogenic induction medium. Taken together, our study provides new insights into the regulatory role of KLF9 in osteogenic differentiation of MSCs.

摘要

骨质疏松症是一种进行性骨骼疾病,其特征是骨量减少和骨微观结构退化。间充质干细胞(MSCs)具有抑制骨质疏松症的潜力,因为它们是多能干细胞,可以分化为多种类型的细胞,包括成骨细胞。因此,MSCs 的成骨分化机制值得全面研究。在这里,我们报告 KLF9 是 MSCs 成骨分化的一个新的调节因子。我们观察到,KLF9 的耗竭可以在很大程度上削弱 MSCs 的成骨分化能力。此外,我们揭示了抑制 PI3K-Akt 通路也会影响成骨分化,因为 KLF9 的耗竭抑制了 PI3K 的表达。最后,我们发现地塞米松可以诱导 KLF9 的表达,地塞米松是成骨诱导培养基中的一个重要组成部分。总之,我们的研究为 KLF9 在 MSCs 成骨分化中的调节作用提供了新的见解。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验