Wnt16 attenuates TGFβ-induced chondrogenic transformation in vascular smooth muscle.

ABSTRACT:

Objective

Phenotypic plasticity of vascular smooth muscle cells (VSMCs) contributes to cardiovascular disease. Chondrocyte-like transformation of VSMCs associates with vascular calcification and underlies the formation of aortic cartilaginous metaplasia induced in mice by genetic loss of matrix Gla protein (MGP). Previous microarray analysis identified a dramatic downregulation of Wnt16 in calcified MGP-null aortae, suggesting an antagonistic role for Wnt16 in the chondrogenic transformation of VSMCs.

Approach and results

Wnt16 is significantly downregulated in MGP-null aortae, before the histological appearance of cartilaginous metaplasia, and in primary MGP-null VSMCs. In contrast, intrinsic TGFβ is activated in MGP-null VSMCs and is necessary for spontaneous chondrogenesi

SUBMITTER: Beazley KE 

PROVIDER: S-EPMC4344425 | biostudies-literature | 2015 Mar

REPOSITORIES: biostudies-literature