Smad2 and myocardin-related transcription factor B cooperatively regulate vascular smooth muscle differentiation from neural crest cells.

ABSTRACT:

Rationale

Vascular smooth muscle cell (VSMC) differentiation from neural crest cells (NCCs) is critical for cardiovascular development, but the mechanisms remain largely unknown.

Objective

Transforming growth factor-β (TGF-β) function in VSMC differentiation from NCCs is controversial. Therefore, we determined the role and mechanism of a TGF-β downstream signaling intermediate Smad2 in NCC differentiation to VSMCs.

Methods and results

By using Cre/loxP system, we generated a NCC tissue-specific Smad2 knockout mouse model and found that Smad2 deletion resulted in defective NCC differentiation to VSMCs in aortic arch arteries during embryonic development and caused vessel wall abnormality in adult carotid arteries where the VSMCs are derived from NCCs. The abnormalities

SUBMITTER: Xie WB 

PROVIDER: S-EPMC3837448 | biostudies-literature | 2013 Sep

REPOSITORIES: biostudies-literature