Smooth muscle-specific Gsα deletion exaggerates angiotensin II-induced abdominal aortic aneurysm formation in mice in vivo.

ABSTRACT:

Objective

Abdominal aortic aneurysm (AAA) is a life-threatening vascular disease without an effective pharmaceutical treatment. Genetic studies have proved the involvement of smooth muscle phenotype switch in the development of AAA. The alpha subunit of the heterotrimeric G stimulatory protein (Gsα) mediates receptor-stimulated production of cyclic adenosine monophosphate (cAMP). However, the role of smooth muscle Gsα in AAA formation remains unknown.

Approach and results

In this study, mice with knockout of smooth muscle-specific Gsα (Gsα^SMKO) were generated by cross-breeding Gsα^flox/flox mice with SM22-CreER^T2 transgenic mice, induced in adult mice by tamoxifen treatment. Gsα deficiency induced a smooth muscle phenotype switch from a contra

SUBMITTER: Qin X 

PROVIDER: S-EPMC7394040 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature