Pharmacologically Improved Contractility Protects Against Aortic Dissection in Mice With Disrupted Transforming Growth Factor-β Signaling Despite Compromised Extracellular Matrix Properties.

ABSTRACT:

Objective

Transforming growth factor-beta is a pleiotropic cytokine having diverse roles in vascular morphogenesis, homeostasis, and pathogenesis. Altered activity of and signaling through transforming growth factor-beta has been implicated in thoracic aortic aneurysms and dissections, conditions characterized by a reduced structural integrity of the wall that associates with altered biomechanics and mechanobiology. We quantify and contrast the passive and active biaxial biomechanical properties of the ascending and proximal descending thoracic aorta in a mouse model of altered transforming growth factor-beta signaling, with and without treatment with rapamycin.

Approach and results

Postnatal disruption of the gene (Tgfbr2) that codes the type II transforming growth factor-b

SUBMITTER: Ferruzzi J 

PROVIDER: S-EPMC4850095 | biostudies-literature | 2016 May

REPOSITORIES: biostudies-literature