Cyclophilin A contributes to aortopathy induced by postnatal loss of smooth muscle TGFBR1.

ABSTRACT: Recent recognition that TGF-β signaling disruption is involved in the development of aortic aneurysms has led to renewed investigations into the role of TGF-β biology in the aortic wall. We previously found that the type I receptor of TGF-β (TGFBR2) receptor contributes to formation of ascending aortic aneurysms and dissections (AADs) induced by smooth muscle cell (SMC)-specific, postnatal deletion of Tgfbr1 (Tgfbr1^iko). Here, we aimed to decipher the mechanistic signaling pathway underlying the pathogenic effects of TGFBR2 in this context. Gene expression profiling demonstrated that Tgfbr1^iko triggers an acute inflammatory response in developing AADs, and Tgfbr1^iko SMCs express an inflammatory phenotype in culture. Comparative p

SUBMITTER: Zhou G 

PROVIDER: S-EPMC6766662 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature