Mechanical stimuli are responsible for bone remodeling during orthodontic tooth movement. The role of mechanical stimulation in the regulation of the fate of bone mesenchymal stem cells (BMSCs) is of interest in bone regeneration and tissue engineering applications. However, the signaling pathway involved in strain-induced biochemical events in BMSCs is not well established and can be controversial. This study investigated strain-induced proliferation and differentiation of BMSCs, as well as the mechanism of mechanotransduction. BMSCs were exposed to continuous mechanical strain (CMS) of 10% at 1 Hz. The results showed that CMS reduced the proliferation of BMSCs and stimulated osteogenic differentiation by activating @entity8087 , followed by increased @entity623 ( @entity623 ) activity and mRNA expression of osteogenesis-related genes ( @entity623 , collagen type I and osteocalcin). Furthermore, the phosphorylation level of extracellular regulated protein kinase ( @entity1366 increased significantly at the onset of strain. However, the presence of @entity5732 , a selective inhibitor of @entity1366 , blocked the induction of @entity8087 and subsequent osteogenic events. These findings demonstrate that CMS regulated @entity8087 activation and favored osteoblast differentiation through activation of the @entity1366 signaling pathway. These results will contribute to a better understanding of strain-induced bone remodeling and will form the basis for the correct choice of applied force in orthodontic treatment.

Osteogenic response of mesenchymal stem cells to continuous mechanical strain is dependent on @entity1366 - XXXX signaling.

@entity5732 :: ('MESH:C113580', 'Chemical') :: ['U0126'] @entity8087 :: ('860', 'Gene') :: ['Runx2'] @entity1366 :: ('5595;5594', 'Gene') :: ['ERK1/2', 'ERK)1/2'] @entity623 :: ('250', 'Gene') :: ['ALP', 'alkaline phosphatase']
@entity8087 :: (860,Gene) :: ['Runx2']
