Mechanical stress modulates bone remodeling signals

摘要: Mechanical stress plays an essential role in bone homeostasis. Although mechanotransduction-induced de novo gene expression is required for remodeling, the molecular mechanism of intracellular signaling, which leads to regulation expression, not fully understood. Here, we show that JNK and p38 [two stress-responsible mitogen-activated protein kinases (MAPKs)] are activated via ASK1 (a MAPK kinase) mechanical stretch loaded MC3T3-E1 preosteoblasts. Using pharmaceutical RNAi approaches, demonstrated Ca2+ influx-induced reactive oxygen species generation. Furthermore, observed ASK1-activated induced two remodeling related genes, Fn14 MCP-3, respectively. These findings suggest stress-activated induce cytokine cross-talks between osteoblasts marrow-derived monocytes macrophages, may play key roles remodeling.