학술논문
Cyclic hydrodynamic pressure induced proliferation of bladder smooth muscle cells via integrin α5 and FAK
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TEXT
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English
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Abstract
T.-Q. Wei ... [et al.].
Obsahuje bibliografii a bibliografické odkazy
According to previous studies, integrins play an important role in the mechanotransduction. The aim of this study was to examine the role of integrin subunits and its down-stream signaling molecules in the cyclic hydrodynamic pressure-induced proliferation of human bladder smooth muscle cells (HBSMCs) cultured in scaffolds. The HBSMCs cultured in scaffolds were subjected to four different levels of cyclic hydrodynamic pressure for 24 hours, which were controlled by a BOSE BioDynamic bioreactor. Flow cytometry was used to examine cell cycle distribution. Real-time RT-PCR and western blotting were used to examine the expression levels of integrin subunits and their downstream signaling molecules. Integrin α 5 siRNA was applied to validate the role of integrin α 5 in cell proliferation. Here, we showed that cyclic hydrodynamic pressure promoted proliferation of HBSMCs. The cyclic hydrodynamic pressure also increased expression of integrin α 5 and phosphorylation of FAK, the key mediator of integrin α 5 signaling, but not that of integrin α 1, α 3, α 4, α v, β 1 and β 3. Moreover, inhibition of integrin α 5 decreased the level of p-FAK and abolished proliferation of HBSMCs stimulated by cyclic hydrodynamic pressure. Taken together, we demonstrate for the fi rst time that the integrin α 5-FAK signaling pathway controls the proliferation of HBSMCs in response to cyclic hydrodynamic pressure.
Obsahuje bibliografii a bibliografické odkazy
According to previous studies, integrins play an important role in the mechanotransduction. The aim of this study was to examine the role of integrin subunits and its down-stream signaling molecules in the cyclic hydrodynamic pressure-induced proliferation of human bladder smooth muscle cells (HBSMCs) cultured in scaffolds. The HBSMCs cultured in scaffolds were subjected to four different levels of cyclic hydrodynamic pressure for 24 hours, which were controlled by a BOSE BioDynamic bioreactor. Flow cytometry was used to examine cell cycle distribution. Real-time RT-PCR and western blotting were used to examine the expression levels of integrin subunits and their downstream signaling molecules. Integrin α 5 siRNA was applied to validate the role of integrin α 5 in cell proliferation. Here, we showed that cyclic hydrodynamic pressure promoted proliferation of HBSMCs. The cyclic hydrodynamic pressure also increased expression of integrin α 5 and phosphorylation of FAK, the key mediator of integrin α 5 signaling, but not that of integrin α 1, α 3, α 4, α v, β 1 and β 3. Moreover, inhibition of integrin α 5 decreased the level of p-FAK and abolished proliferation of HBSMCs stimulated by cyclic hydrodynamic pressure. Taken together, we demonstrate for the fi rst time that the integrin α 5-FAK signaling pathway controls the proliferation of HBSMCs in response to cyclic hydrodynamic pressure.