The Role Of BRCC36 In Pulmonary Artery Smooth Muscle Cells In Mediating CGMP Inhibition Of TGF-β Signaling

Objective:The present project aims to investigate the effects of BRCC36 in cGMP Inhibiting TGF-Signaling and proboly mechanism.Methods:(l)PASMCs were treated with cGMP,and then was subjected to TGF-01 treatment, we detected the expression of PAI-1 by using RT-PCR.(2)PASMCs were treated with TGF-β1 for 12h,and then we detected the expression of BRCC36 by western bolt.(3)PASMCs were treated with overexpression of BRCC36 adenovirus or null adenovirus, and treated with cGMP, and then was subjected to TGF-01 treatment,.we detected the expression of PAI-1 by using RT-PCR.(4)PASMCs were treated with overexpression of BRCC36 adencvirus and treated with Nocodazole、cGMP and then was subjected to TGF-β1 treatment, we detected the expression of PAI-1 by using RT-PCRResults:(1) In PASMCs,cGMP Inhibits TGF-Signaling-induced PAI-1 mRNA expression.(2) In PASMCs,When treated with TGF-β1, expression of BRCC36 was increased.(2) In PASMCs, overexpression BRCC36 can enhance the inhibitory effect of cGMP on TGF-β1 signaling.(3)Nocodazole pretreatment abolishes BRCC36 enhancing the inhibitory effect of cGMP on TGF-β1-induced PAI-1 mRNA expression.Conclusion:BRCC36 can enhances the inhibitory effect of cGMP on TGF-β1 signaling,by sequestering Smad3 with Cytosolic 2-Tubulin in Pulmonary Artery Smooth Muscle Cells...