中文摘要：

为了证实JNK激酶在骨形态发生蛋白9（bone morphogenetic proteins 9,BMP9） 诱导间充质干细胞C3H10T1/2成骨分化中的作用,利用重组腺病毒将BMP9导入间充质干细胞C3H10T1/2. 通过碱性磷酸酶（ALP）活性测定、钙盐沉积实验、荧光素酶报告基因检测、Western印迹和组织化学染色等方法，检测BMP9是否可经JNK激酶途径调控间充质干细胞C3H10T1/2向成骨分化.动物实验验证在RNA沉默JNK蛋白激酶后，对BMP9诱导间充质干细胞C3H10T1/2向成骨分化的影响．结果发现，BMP9可以增强JNK 激酶的磷酸化；利用JNK抑制剂SP600125抑制JNK激酶活性后，BMP9诱导的间充质干细胞C3H10T1/2的早期成骨指标ALP活性和晚期指标钙盐沉积均受到抑制，而且经典SMAD信号的活化也相应受到抑制；RNA干扰沉默JNK基因表达后，同样也可抑制BMP9 诱导的C3H10T1/2细胞的ALP活性和裸鼠皮下异位成骨．因此表明，BMP9可活化JNK激酶途径从而诱导间充质干细胞C3H10T1/2向成骨分化．

英文摘要：

To confirm the effects of JNK on BMP9-induced osteogenic differentiation in C3H10T1/2 mesenchymal stem cells, C3H10T1/2 cells were infected by recombinant adenovirus BMP9. Alkaline phosphatase （ALP） activity assay, calcium deposition staining, luciferase activity assay, Western blotting and histochemical staining were used to investigate whether BMP9 could induce osteogenic differentiation of C3H10T1/2 mesenchymal stem cells through the JNK kinase pathway. Animal assay was accomplished to testify that whether blockage of JNK kinase can result in inhibition of entopic bone formation induced by BMP9 in vivo.It was found that BMP9 could increase the phosphorylated form of JNK kinase and JNK kinase inhibitor SP600125 could suppress BMP9-induced early osteogenic marker, such as alkaline phosphatase （ALP）, and late osteogenic markers, such as calcium deposition.Moreover, activation of canonical Smad signaling was also inhibited by SP600125.Furthermore, inhibition of JNK activity was shown to decrease ALP activity and lead to significant decrease in entopic bone formation in vivo.These results suggested that BMP9 can induce osteogenic differentiation of C3H10T1/2 mesenchymal stem cells through the JNK kinase pathway.