Abca1 deficiency protects the heart against myocardial infarction-induced injury

Abstract

Background and aims: We explored the role of ATP-binding cassette transporter A1 (Abca1), in post-myocardial infarction (MI) cardiac injury.

Methods: In Abca1(-/-) mice, wild type (WT) mice, and WT mice transplanted with Abca1(-/-) or WT bone marrow, an MI was induced in vivo. Furthermore, an ex vivo MI was induced in isolated Abca1(-/-) and WT hearts.

Results: Twenty-four hours and two weeks after in vivo MI induction, MI size was reduced in Abca1(-/-) (-58%, p = 0.007; -59%, p = 0.03) compared to WT. Ex vivo MI induction showed no effect of Abca1(-/-) on infarct size. Interestingly, two weeks after MI, Abca1(-/-) mice showed higher circulating levels of B-cells (+3.0 fold, p = 0.02) and T-cells (+4.2 fold, p = 0.002) compared to WT. Bone marrow-specific Abca1(-/-) tended to reduce infarct size (-43%, p = 0.12), suggesting a detrimental role for hematopoietic Abca1 after MI.

Conclusions: Although Abca1 has a protective role in atherosclerosis, it exerts detrimental effects on cardiac function after MI.

Keywords: Abca1 deficiency; Immune cells; Mice; Myocardial infarction.