Shift toward greater pathologic post-myocardial infarction remodeling with loss of the adaptive hypertrophic signaling of alpha1 adrenergic receptors in mice.

ABSTRACT:

Rationale

We have hypothesized that post-infarction cardiac remodeling can be influenced by shifts in the balance between intracellular mediators of "pathologic" and "physiologic" hypertrophy. Although alpha1 adrenergic receptors (alpha1-ARs) mediate pro-adaptive hypertrophy during pressure overload, little is known about their role or downstream mediators after myocardial infarction.

Methods

We performed loss-of-function experiments via coronary ligation in alpha1A-AR knockout (AKO) mice. Post-myocardial infarction (MI) remodeling was evaluated via echocardiography, quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis of cardiac fetal gene expression, histologic analysis of myocyte size, post-MI fibrosis and apoptosis, and Western blot analysis of

SUBMITTER: Yeh CC 

PROVIDER: S-EPMC5720786 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature