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Abca1 deficiency protects the heart against myocardial infarction-induced injury
Louwe, M.C.; Lammers, B.; Frias, M.A.; Foks, A.C.; Leeuw, L.R. de; Hildebrand, R.B.; ... ; Eck, M. van 2016
Abca1 deficiency protects the heart against myocardial infarction-induced injury
Article / Letter to editor
metadata only
Conclusions: Although Abca1 has a protective role in atherosclerosis, it exerts detrimental effects on cardiac function after MI. (C) 2016 The Authors. Published by Elsevier Ireland Ltd. This is an... Show moreConclusions: Although Abca1 has a protective role in atherosclerosis, it exerts detrimental effects on cardiac function after MI. (C) 2016 The Authors. Published by Elsevier Ireland Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Show less
ABCA1 deficiency protects the heart against myocardial infarction-induced injury
Louwe, M.C.; Lammers, B.; Frias, M.A.; Foks, A.C.; Leeuw, L.R. de.; Hildebrand, R.B.; ... ; Eck, M. van 2016
ABCA1 deficiency protects the heart against myocardial infarction-induced injury
Article / Letter to editor
open access
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... Show more

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;
  • Myocardial infarction;
  • Immune cells;
  • Mice

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Diabetes Mellitus Is Associated With Reduced High-Density Lipoprotein Sphingosine-1-Phosphate Content and Impaired High-Density Lipoprotein Cardiac Cell Protection
Brinck, J.W.; Thomas, A.; Lauer, E.; Jornayvaz, F.R.; Brulhart-Meynet, M-C.; Prost, J-C.; ... ; Frias Miguel, A. 2016
Diabetes Mellitus Is Associated With Reduced High-Density Lipoprotein Sphingosine-1-Phosphate Content and Impaired High-Density Lipoprotein Cardiac Cell Protection
Article / Letter to editor
metadata only
OBJECTIVE: The dyslipidemia of type 2 diabetes mellitus has multiple etiologies and impairs lipoprotein functionality, thereby increasing risk for cardiovascular disease. High-density lipoproteins ... Show moreOBJECTIVE: The dyslipidemia of type 2 diabetes mellitus has multiple etiologies and impairs lipoprotein functionality, thereby increasing risk for cardiovascular disease. High-density lipoproteins (HDLs) have several beneficial effects, notably protecting the heart from myocardial ischemia. We hypothesized that glycation of HDL could compromise this cardioprotective effect.APPROACH AND RESULTS: We used in vitro (cardiomyocytes) and ex vivo (whole heart) models subjected to oxidative stress together with HDL isolated from diabetic patients and nondiabetic HDL glycated in vitro (methylglyoxal). Diabetic and in vitro glycated HDL were less effective (P<0.05) than control HDL in protecting from oxidative stress. Protection was significantly, inversely correlated with the degree of in vitro glycation (P<0.001) and the levels of hemoglobin A1c in diabetic patients (P<0.007). The ability to activate protective, intracellular survival pathways involving Akt, Stat3, and Erk1/2 was significantly reduced (P<0.05) using glycated HDL. Glycation reduced the sphingosine-1-phosphate (S1P) content of HDL, whereas the S1P concentrations of diabetic HDL were inversely correlated with hemoglobin A1c (P<0.005). The S1P contents of in vitro glycated and diabetic HDL were significantly, positively correlated (both <0.01) with cardiomyocyte survival during oxidative stress. Adding S1P to diabetic HDL increased its S1P content and restored its cardioprotective function.CONCLUSIONS: Our data demonstrate that glycation can reduce the S1P content of HDL, leading to increased cardiomyocyte cell death because of less effective activation of intracellular survival pathways. It has important implications for the functionality of HDL in diabetes mellitus because HDL-S1P has several beneficial effects on the vasculature. Show less
Abca1 deficiency protects the heart against myocardial infarction-induced injury
Louwe, M.C.; Lammers, B.; Frias, M.A.; Foks, A.C.; Leeuw, L.R. de; Hildebrand, R.B.; ... ; Eck, M. van 2016
Abca1 deficiency protects the heart against myocardial infarction-induced injury
Article / Letter to editor
open access
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... 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 Show less