Li X L, Liu Y B, Ma E G, Shen W X, Li H, Zhang Y N
The Cadre Ward, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Department of Cardiology, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Genet Mol Res. 2015 Jul 13;14(3):7605-15. doi: 10.4238/2015.July.13.4.
We investigated the synergistic effect of bone morphogenetic protein 9 (BMP9) and transforming growth factor (TGF)-b in the transformation of mesenchymal stem cells into osteoblasts. We evaluated the effect of BMP9 and TGF-b on the induction of osteoblast formation. Mitogen-activated protein kinase (MAPK) pathway-related proteins such as p38, extracellular receptor kinase 1/2, and c-Jun N-terminal kinase (JNK) were analyzed. The interactions between TGF-Smad and BMP-MAPK were also studied. BMP9 alone induced the differentiation of mesenchymal stem cells (MSCs) into osteoblasts and enhanced phosphorylation of p38, extracellular receptor kinase 1/2, and JNK. TGF-b alone failed to induce transformation, but could increase the effect of BMP9. In this process the activation of Smad resulted in activation of the JNK pathway in the MAPK pathway. BMP9 induced osteogenesis of MSC differentiation through the MAKP pathway, while TGF-b contributed to BMP9 enhancement through the Smad-JNK pathway.
我们研究了骨形态发生蛋白9（BMP9）和转化生长因子（TGF）-β在间充质干细胞向成骨细胞转化中的协同作用。我们评估了BMP9和TGF-β对成骨细胞形成诱导的影响。分析了丝裂原活化蛋白激酶（MAPK）途径相关蛋白，如p38、细胞外受体激酶1/2和c-Jun氨基末端激酶（JNK）。还研究了TGF-Smad和BMP-MAPK之间的相互作用。单独的BMP9可诱导间充质干细胞（MSC）分化为成骨细胞，并增强p38、细胞外受体激酶1/2和JNK的磷酸化。单独的TGF-β未能诱导转化，但可增强BMP9的作用。在此过程中，Smad的激活导致MAPK途径中JNK途径的激活。BMP9通过MAKP途径诱导MSC分化的成骨作用，而TGF-β通过Smad-JNK途径促进BMP9的增强作用。
