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结构退化。间充质干细胞（MSC）具有抑制骨质疏松症的潜力，因为它们是可以分化为包括成骨细胞在内的多种类型细胞的多能干细胞。因此，MSCs成骨分化的机制值得全面研究。在这里，我们报道KLF9是MSCs成骨分化的一种新型调节因子。我们观察到KLF9的消耗可以在很大程度上损害MSCs的成骨分化能力。此外,我们发现抑制PI3K-Akt通路也可影响成骨分化,因为KLF9耗竭抑制PI3K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重要成分。一起来看,我们的研究为KLF9在MSCs成骨分化中的调控作用提供了新的见解。
