Aib1 deficiency exacerbates inflammatory responses in acute myocardial infarction mice.

Abstract

Acute myocardial infarction (AMI) is one of the major causes of death throughout the world, while inflammation has been known as a major contributor to the pathophysiology of AMI. Inhibition of inflammation is shown to protect from AMI. Amplified in breast 1 (Aib1) is a transcriptional coactivator protein which can suppress inflammation. The anti-inflammatory activities of Aib1 imply its potential effects against AMI; however, to date the role of Aib1 in AMI has not been described yet. Here we explored the potential functions of Aib1 in AMI. We induced AMI in both wild-type (WT) and Aib1-/- mice. The expression levels of Aib1 and inflammatory cytokines in the AMI WT mice were measured by RT-PCR and Western blot. The heart infarction area and cardiac functions were compared between the AMI WT and Aib1-/- mice. The expression levels of inflammatory cytokines including IL-6, IL-1β, TNF-α, and MCP-1 in heart tissues were compared between the AMI WT and Aib1-/- mice by ELISA and RT-PCR. AMI induced the production of inflammatory cytokines whereas suppressed the expression of Aib1 in WT mice. AMI Aib1-/- mice displayed increased infarct area and aggravated heart dysfunction, as well as upregulated levels of Il-6, Il-1β, Tnf-α, and Mcp-1 in heart tissues. Aib1 deficiency exacerbates inflammation in AMI mice. KEY MESSAGES: AMI induced inflammation in the heart tissue of mice. Aib1 knockout exacerbated infarction in AMI mice. Aib1 knockout exacerbated cardiac dysfunction in AMI mice. Aib1 knockout exacerbated inflammation in AMI mice.