Bone morphogenetic proteins (BMPs), have been shown to enhance the osteogenic differentiation of mesenchymal cells (MCs) and to promote bone formation. BMP6 is known to play an important role in the process of MCs towards osteogenic differentiation by virtue of their osteoinductive and cell type specific proliferative activity. However, the molecular mechanism relate to BMP6 osteoinductive activity is still unclear and continues to warrant further investigation. Msx2 is a member of the homeobox gene family of transcription factors and promotes calcification. Hence, we wondered if it might also play a role in BMP6-induced osteogenesis. In this study, two mouse mesenchymal cell lines were treated with BMP6, adenovirus-Msx2 (Ad-Msx2) or adenovirus-siMsx2 (Ad-siMsx2). Based on the results of mRNA and protein expression, it was indicated that BMP6 could enhance the expression of Msx2 and activate the phosphorylation of Smad 1/5/8, p38 and ERK1/2. Being transfected by Ad-Msx2, the BMP6-induced activation of phosphorylation was significantly promoted. On the contrary, two cell lines transfected by Ad-siMsx2 presented an inhibited expression of three phosphorylated proteins even after being induced by BMP6. The evaluation of ALP, OPN, OC and calcium deposits revealed the osteogenic results those were corresponding to the results of mRNA and protein. Taken together, these findings can be a novel viewpoint for the understanding of the mechanisms of BMP6-induced osteogenesis and provide therapeutic targets of bone defect.

骨形态发生蛋白（BMP）已显示出增强间充质细胞（MCs）的成骨分化并促进骨形成。已知BMP6凭借其骨诱导和细胞类型特异性增殖活性，在MCs向成骨分化的过程中起重要作用。但是，与BMP6骨诱导活性有关的分子机制仍不清楚，并且仍需进一步研究。Msx2是转录因子同源异型盒基因家族的成员，并促进钙化。因此，我们想知道它是否也可能在BMP6诱导的成骨中起作用。在这项研究中，两种小鼠间充质细胞系分别用BMP6，腺病毒-Msx2（Ad-Msx2）或腺病毒-siMsx2（Ad-siMsx2）处理。根据mRNA和蛋白质表达的结果，提示BMP6可以增强Msx2的表达并激活Smad 1/5/8，p38和ERK1 / 2的磷酸化。通过Ad-Msx2转染，BMP6诱导的磷酸化激活得到显着促进。相反，即使在被BMP6诱导后，被Ad-siMsx2转染的两个细胞系也呈现出三种磷酸化蛋白的抑制表达。对ALP，OPN，OC和钙沉积物的评估表明，成骨结果与mRNA和蛋白质的结果相对应。综上所述，这些发现可能是了解BMP6诱导成骨机制的新观点，并提供了骨缺损的治疗靶点。BMP6诱导的磷酸化激活得到显着促进。相反，被Ad-siMsx2转染的两个细胞系即使在被BMP6诱导后，也表现出三种磷酸化蛋白表达的抑制。对ALP，OPN，OC和钙沉积物的评估表明，成骨结果与mRNA和蛋白质的结果相对应。综上所述，这些发现可能是了解BMP6诱导成骨机制的新观点，并提供了骨缺损的治疗靶点。BMP6诱导的磷酸化激活得到显着促进。相反，被Ad-siMsx2转染的两个细胞系即使在被BMP6诱导后，也表现出三种磷酸化蛋白表达的抑制。对ALP，OPN，OC和钙沉积物的评估表明，成骨结果与mRNA和蛋白质的结果相对应。综上所述，这些发现可能是理解BMP6诱导成骨机制的新观点，并提供了骨缺损的治疗靶点。OC和钙沉积物显示出成骨结果，这些结果与mRNA和蛋白质的结果相对应。综上所述，这些发现可能是了解BMP6诱导成骨机制的新观点，并提供了骨缺损的治疗靶点。OC和钙沉积物显示出成骨结果，这些结果与mRNA和蛋白质的结果相对应。综上所述，这些发现可能是了解BMP6诱导成骨机制的新观点，并提供了骨缺损的治疗靶点。