作者: Bing Tu , Shen Liu , Guangwang Liu , Zhiwei Li , Yangbai Sun
DOI: 10.1038/SREP37184
关键词:
摘要: Heterotopic ossification (HO) can result from traumatic injury, surgery or genetic diseases. Here, we demonstrate that overexpression of connexin 43 (Cx43) is critical for the development and recurrence HO in patients. Inhibition Cx43 by shRNA substantially suppressed osteogenic differentiation MC-3T3 cells expression genes. We employed a tenotomy mouse model to explore hypothesis vital HO. specific decreased extraskeletal bone formation vivo. In addition, demonstrated ERK signaling activated plays an important role promoting was highly tissue collected patient models. Importantly, de novo soft significantly attenuated mice treated with U0126. led expressions Runx2, BSP Col-1 vivo vitro. Moreover, patients low activation had lower risk after lesions were surgically removed. Our findings indicate promotes trauma-induced activating pathway enhances markers.