Protease-activated receptor 2 deficient mice develop less angiotensin II induced left ventricular hypertrophy but more cardiac fibrosis.

ABSTRACT:

Aims

Activation of Protease Activated Receptor 2 (PAR2) has been shown to be involved in regulation of injury-related processes including inflammation, fibrosis and hypertrophy. In this study we will investigate the role of PAR2 in cardiac injury in a mouse model of hypertension using continuous infusion with angiotensin II.

Methods

Hypertension was induced in 12 weeks old wildtype (wt, n = 8) and PAR2 deficient mice (n = 9) by continuous infusion with angiotensin II for 4 weeks using osmotic minipumps. At the end, hearts were collected for analysis of left ventricular hypertrophy (LVH), myocardial capillary supply, fibrosis and localization of PAR2 expression using histological, immunohistological and mRNA expression analysis techniques. In addition, rat cardiac fibroblasts

SUBMITTER: Meyer Zu Schwabedissen A 

PROVIDER: S-EPMC11620577 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature