抄録
Human mesenchymal stem cells (hMSCs) are expected to use as vehicles for delivering therapeutic genes to sites of injury and exposed to shear stress in that situation. However, the effect of fluid shear stress on the migration and the mechanisms are both limited. Using a parallel plate flow chamber system, we applied steady shear stress of 0.2 ～ 6 Pa to fluorescently labelled hMSCs. Cell migration was evaluated by the rate of wound area in the scratch injury assay. In the absence of flow (control), cells reached confluence at 10 h after wound performed. Under shear stress of 0.2 Pa, it was clear that flow stimulation caused notably faster wound closure than the control, which showed confluence at 6 h, while there was no significant difference in the migration of 0.5 Pa and 1 Pa shear stress groups compared with the control. Cell migration was prominently inhibited in higher shear stresses than 2 Pa. To understand the mechanisms the inhibitory experiments for MAPK family were carried out. The results suggest that JNK inhibitor abolished the effect of shear stress on migration of hMSCs, indicating that JNK plays a prominent role in shear stress-induced migration of hMSCs than ERK.
