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ABCA1 deficiency protects the heart against myocardial infarction-induced injury
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...
Show moreBackground 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;
- Myocardial infarction;
- Immune cells;
- Mice
- All authors
- Louwe, M.C.; Lammers, B.; Frias, M.A.; Foks, A.C.; Leeuw, L.R. de.; Hildebrand, R.B.; Kuiper, J.; Smit, J.W.A.; Berkel, T.J.C. van; James, R.W.; Geerling, J.J.; Rensen, P.C.N.; Eck, M. van
- Date
- 2016-06-11
- Journal
- Atherosclerosis
- Volume
- 251
- Pages
- 159 - 163