KLF9 regulates osteogenic differentiation of mesenchymal stem cells

IF 2.9 4区生物学 Q3 CELL BIOLOGY

Journal of Molecular Histology Pub Date : 2024-05-27 DOI:10.1007/s10735-024-10204-6

Xiaoxiao Xiao, Ming Zhang, Yiwei Qian, Xuepeng Wang, Qiang Wu

引用次数: 0

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.

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KLF9 可调节间充质干细胞的成骨分化。

骨质疏松症是一种渐进性骨骼疾病，其特征是骨量减少和骨微结构退化。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，可以分化成多种类型的细胞，包括成骨细胞。因此，间充质干细胞的成骨分化机制值得全面研究。在此，我们报告了KLF9是间充质干细胞成骨分化过程中的新型调节因子。我们观察到，消耗 KLF9 在很大程度上会影响间充质干细胞的成骨分化能力。此外，我们还发现抑制 PI3K-Akt 通路也会影响成骨分化，因为 KLF9 的耗竭会抑制 PI3K 的表达。最后，我们发现地塞米松可以诱导 KLF9 的表达，而地塞米松是成骨诱导培养基的重要成分。综上所述，我们的研究为 KLF9 在间充质干细胞成骨分化中的调控作用提供了新的见解。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Molecular Histology 生物-细胞生物学

CiteScore

5.90

自引率

0.00%

发文量

审稿时长

1 months

期刊介绍： The Journal of Molecular Histology publishes results of original research on the localization and expression of molecules in animal cells, tissues and organs. Coverage includes studies describing novel cellular or ultrastructural distributions of molecules which provide insight into biochemical or physiological function, development, histologic structure and disease processes. Major research themes of particular interest include: - Cell-Cell and Cell-Matrix Interactions; - Connective Tissues; - Development and Disease; - Neuroscience. Please note that the Journal of Molecular Histology does not consider manuscripts dealing with the application of immunological or other probes on non-standard laboratory animal models unless the results are clearly of significant and general biological importance. The Journal of Molecular Histology publishes full-length original research papers, review articles, short communications and letters to the editors. All manuscripts are typically reviewed by two independent referees. The Journal of Molecular Histology is a continuation of The Histochemical Journal.