ArticleArteriosclerosis, thrombosis, and vascular biology2016
Deficiency of ATP-Binding Cassette Transporters A1 and G1 in Endothelial Cells Accelerates Atherosclerosis in Mice.
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Article in Arteriosclerosis, thrombosis, and vascular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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60citing papers in PubMed
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60 citing papers in PubMed, 112 citations in OpenAlex.
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- Identification of key genes related to macrophages and metabolic reprogramming in myocardial infarct based on single-cell and bulk transcriptomics data and experimental validation.BMC cardiovascular disorders · 2026Article
- Cholesterol efflux protein, ABCA1, supports anticancer functions of myeloid immune cells.Science advances · 2026Article
- HDLR-SR-BI Expression and Cholesterol Uptake are Regulated via Indoleamine-2,3-dioxygenase 1 in Macrophages under Inflammation.Langmuir : the ACS journal of surfaces and colloids · 2025Article
- Overexpression of ABCA1 in Carotid Endothelium of Hyperlipidemic Rabbits Modulates Vascular Inflammation.Human gene therapy · 2025Article
- SMC Abca1 and Abcg1 Deficiency Enhances Urinary Bladder Distension but Not Atherosclerosis.Circulation research · 2025Article
- Inhibiting MiR-33a-3p Expression Fails to Enhance ApoAI-Mediated Cholesterol Efflux in Pro-Inflammatory Endothelial Cells.Medicina (Kaunas, Lithuania) · 2025Article
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- Cholesterol Efflux Decreases TLR4-Target Gene Expression in Cultured Macrophages Exposed toMicroorganisms · 2024Article
- Rewiring Endothelial Sphingolipid Metabolism to Favor S1P Over Ceramide Protects From Coronary Atherosclerosis.Circulation research · 2024Article
- Dissecting the Impact of Vascular Smooth Muscle Cell ABCA1 versus ABCG1 Expression on Cholesterol Efflux and Macrophage-like Cell Transdifferentiation: The Role of SR-BI.Journal of cardiovascular development and disease · 2023Article
- High-density lipoprotein regulates angiogenesis by long non-coding RNA HDRACA.Signal transduction and targeted therapy · 2023Article
- The Impact of MiR-33a-5p Inhibition in Pro-Inflammatory Endothelial Cells.Diseases (Basel, Switzerland) · 2023Article
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- Epsin Nanotherapy Regulates Cholesterol Transport to Fortify Atheroma Regression.Circulation research · 2023Article
- Administration of an LXR agonist promotes atherosclerotic lesion remodelling in murine inflammatory arthritis.Clinical & translational immunology · 2023Article
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- MiR-199a-3p Restrains Foaming and Inflammation by Regulating RUNX1 in Macrophages.Molecular biotechnology · 2022Article
- Baicalein inhibits macrophage lipid accumulation and inflammatory response by activating the PPARγ/LXRα pathway.Clinical and experimental immunology · 2022Article
- Inflammatory stress signaling via NF-eLife · 2022Article
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Authors and funding
13 authors at 2 institutions in 2 countries.
Marit WesterterpFrom the Division of Molecular Medicine, Department of Medicine (M.W., P.F., A.E.B., M.M.M., V.N., S.A., C.L.W., A.R.T.), Naomi Berrie Diabetes Center (K.T., D.A.), and Department of Pathology, Obstetrics, and Gynaecology (I.W.T., J.K.), Columbia University, New York, NY; Section on Molecular Genetics, Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands (M.W.); Department of Diabetes, Endocrinology, and Metabolism, Medical Hospital of Tokyo Medical and Dental University, Tokyo, Japan (K.T.); and Section on Molecular Medicine, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC (J.S.P.). mw2537@columbia.edu.
Kyoichiro TsuchiyaFrom the Division of Molecular Medicine, Department of Medicine (M.W., P.F., A.E.B., M.M.M., V.N., S.A., C.L.W., A.R.T.), Naomi Berrie Diabetes Center (K.T., D.A.), and Department of Pathology, Obstetrics, and Gynaecology (I.W.T., J.K.), Columbia University, New York, NY; Section on Molecular Genetics, Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands (M.W.); Department of Diabetes, Endocrinology, and Metabolism, Medical Hospital of Tokyo Medical and Dental University, Tokyo, Japan (K.T.); and Section on Molecular Medicine, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC (J.S.P.).
Ian W TattersallFrom the Division of Molecular Medicine, Department of Medicine (M.W., P.F., A.E.B., M.M.M., V.N., S.A., C.L.W., A.R.T.), Naomi Berrie Diabetes Center (K.T., D.A.), and Department of Pathology, Obstetrics, and Gynaecology (I.W.T., J.K.), Columbia University, New York, NY; Section on Molecular Genetics, Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands (M.W.); Department of Diabetes, Endocrinology, and Metabolism, Medical Hospital of Tokyo Medical and Dental University, Tokyo, Japan (K.T.); and Section on Molecular Medicine, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC (J.S.P.).
Panagiotis FotakisFrom the Division of Molecular Medicine, Department of Medicine (M.W., P.F., A.E.B., M.M.M., V.N., S.A., C.L.W., A.R.T.), Naomi Berrie Diabetes Center (K.T., D.A.), and Department of Pathology, Obstetrics, and Gynaecology (I.W.T., J.K.), Columbia University, New York, NY; Section on Molecular Genetics, Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands (M.W.); Department of Diabetes, Endocrinology, and Metabolism, Medical Hospital of Tokyo Medical and Dental University, Tokyo, Japan (K.T.); and Section on Molecular Medicine, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC (J.S.P.).
Andrea E BochemFrom the Division of Molecular Medicine, Department of Medicine (M.W., P.F., A.E.B., M.M.M., V.N., S.A., C.L.W., A.R.T.), Naomi Berrie Diabetes Center (K.T., D.A.), and Department of Pathology, Obstetrics, and Gynaecology (I.W.T., J.K.), Columbia University, New York, NY; Section on Molecular Genetics, Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands (M.W.); Department of Diabetes, Endocrinology, and Metabolism, Medical Hospital of Tokyo Medical and Dental University, Tokyo, Japan (K.T.); and Section on Molecular Medicine, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC (J.S.P.).
Matthew M MoluskyFrom the Division of Molecular Medicine, Department of Medicine (M.W., P.F., A.E.B., M.M.M., V.N., S.A., C.L.W., A.R.T.), Naomi Berrie Diabetes Center (K.T., D.A.), and Department of Pathology, Obstetrics, and Gynaecology (I.W.T., J.K.), Columbia University, New York, NY; Section on Molecular Genetics, Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands (M.W.); Department of Diabetes, Endocrinology, and Metabolism, Medical Hospital of Tokyo Medical and Dental University, Tokyo, Japan (K.T.); and Section on Molecular Medicine, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC (J.S.P.).
Vusisizwe NtongaFrom the Division of Molecular Medicine, Department of Medicine (M.W., P.F., A.E.B., M.M.M., V.N., S.A., C.L.W., A.R.T.), Naomi Berrie Diabetes Center (K.T., D.A.), and Department of Pathology, Obstetrics, and Gynaecology (I.W.T., J.K.), Columbia University, New York, NY; Section on Molecular Genetics, Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands (M.W.); Department of Diabetes, Endocrinology, and Metabolism, Medical Hospital of Tokyo Medical and Dental University, Tokyo, Japan (K.T.); and Section on Molecular Medicine, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC (J.S.P.).
Sandra AbramowiczFrom the Division of Molecular Medicine, Department of Medicine (M.W., P.F., A.E.B., M.M.M., V.N., S.A., C.L.W., A.R.T.), Naomi Berrie Diabetes Center (K.T., D.A.), and Department of Pathology, Obstetrics, and Gynaecology (I.W.T., J.K.), Columbia University, New York, NY; Section on Molecular Genetics, Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands (M.W.); Department of Diabetes, Endocrinology, and Metabolism, Medical Hospital of Tokyo Medical and Dental University, Tokyo, Japan (K.T.); and Section on Molecular Medicine, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC (J.S.P.).
John S ParksFrom the Division of Molecular Medicine, Department of Medicine (M.W., P.F., A.E.B., M.M.M., V.N., S.A., C.L.W., A.R.T.), Naomi Berrie Diabetes Center (K.T., D.A.), and Department of Pathology, Obstetrics, and Gynaecology (I.W.T., J.K.), Columbia University, New York, NY; Section on Molecular Genetics, Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands (M.W.); Department of Diabetes, Endocrinology, and Metabolism, Medical Hospital of Tokyo Medical and Dental University, Tokyo, Japan (K.T.); and Section on Molecular Medicine, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC (J.S.P.).
Carrie L WelchFrom the Division of Molecular Medicine, Department of Medicine (M.W., P.F., A.E.B., M.M.M., V.N., S.A., C.L.W., A.R.T.), Naomi Berrie Diabetes Center (K.T., D.A.), and Department of Pathology, Obstetrics, and Gynaecology (I.W.T., J.K.), Columbia University, New York, NY; Section on Molecular Genetics, Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands (M.W.); Department of Diabetes, Endocrinology, and Metabolism, Medical Hospital of Tokyo Medical and Dental University, Tokyo, Japan (K.T.); and Section on Molecular Medicine, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC (J.S.P.).
Jan KitajewskiFrom the Division of Molecular Medicine, Department of Medicine (M.W., P.F., A.E.B., M.M.M., V.N., S.A., C.L.W., A.R.T.), Naomi Berrie Diabetes Center (K.T., D.A.), and Department of Pathology, Obstetrics, and Gynaecology (I.W.T., J.K.), Columbia University, New York, NY; Section on Molecular Genetics, Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands (M.W.); Department of Diabetes, Endocrinology, and Metabolism, Medical Hospital of Tokyo Medical and Dental University, Tokyo, Japan (K.T.); and Section on Molecular Medicine, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC (J.S.P.).
Domenico AcciliFrom the Division of Molecular Medicine, Department of Medicine (M.W., P.F., A.E.B., M.M.M., V.N., S.A., C.L.W., A.R.T.), Naomi Berrie Diabetes Center (K.T., D.A.), and Department of Pathology, Obstetrics, and Gynaecology (I.W.T., J.K.), Columbia University, New York, NY; Section on Molecular Genetics, Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands (M.W.); Department of Diabetes, Endocrinology, and Metabolism, Medical Hospital of Tokyo Medical and Dental University, Tokyo, Japan (K.T.); and Section on Molecular Medicine, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC (J.S.P.).
Alan R TallFrom the Division of Molecular Medicine, Department of Medicine (M.W., P.F., A.E.B., M.M.M., V.N., S.A., C.L.W., A.R.T.), Naomi Berrie Diabetes Center (K.T., D.A.), and Department of Pathology, Obstetrics, and Gynaecology (I.W.T., J.K.), Columbia University, New York, NY; Section on Molecular Genetics, Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands (M.W.); Department of Diabetes, Endocrinology, and Metabolism, Medical Hospital of Tokyo Medical and Dental University, Tokyo, Japan (K.T.); and Section on Molecular Medicine, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC (J.S.P.).
University Medical Center Groningen · NLTokyo Medical and Dental University Hospital · JP
Funding
TTC39B in obesity and atherosclerosisP01HL087123 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TALL, ALAN RICHARD · 2007 to 2022
$31.2MPOSTDOCTORAL TRAINING IN ARTERIOSCLEROSIS RESEARCHT32HL007343 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI HENRY N GINSBERG, Muredach P Reilly · 1985 to 2026
$12.7MCholesterol efflux, CHIP and inflammasome activationR01HL107653 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ALAN richard TALL · 2011 to 2026
$7.7MNotch in Angiogenesis and Vascular BiologyR01HL112626 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Jan K. Kitajewski · 2012 to 2026
$6.3MThe Role of Hepatocyte ABCA1 in Lipid Mobilization and TransportR01HL119962 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI PARKS, JOHN S · 2013 to 2022
$3.9MCLIC Function In AngiogenesisR01HL119043 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI KITAJEWSKI, JAN K. · 2014 to 2017
$1.7MBecton Dickinson LSR II Analytical Flow CytometerS10RR027050 · NCRR · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI CLYNES, RAPHAEL A. · 2011 to 2011
$413kNCRR NIH HHS S10 RR027050NHLBI NIH HHS P01 HL087123NHLBI NIH HHS R01 HL107653NHLBI NIH HHS R01 HL112626NHLBI NIH HHS R01 HL119043NHLBI NIH HHS R01 HL119962NHLBI NIH HHS T32 HL007343
Abstract
objectivePlasma high-density lipoproteins have several putative antiatherogenic effects, including preservation of endothelial functions. This is thought to be mediated, in part, by the ability of high-density lipoproteins to promote cholesterol efflux from endothelial cells (ECs). The ATP-binding cassette transporters A1 and G1 (ABCA1 and ABCG1) interact with high-density lipoproteins to promote cholesterol efflux from ECs. To determine the impact of endothelial cholesterol efflux pathways on atherogenesis, we prepared mice with endothelium-specific knockout of Abca1 and Abcg1. APPROACH AND
resultsGeneration of mice with EC-ABCA1 and ABCG1 deficiency required crossbreeding Abca1(fl/fl)Abcg1(fl/fl)Ldlr(-/-) mice with the Tie2Cre strain, followed by irradiation and transplantation of Abca1(fl/fl)Abcg1(fl/fl) bone marrow to abrogate the effects of macrophage ABCA1 and ABCG1 deficiency induced by Tie2Cre. After 20 to 22 weeks of Western-type diet, both single EC-Abca1 and Abcg1 deficiency increased atherosclerosis in the aortic root and whole aorta. Combined EC-Abca1/g1 deficiency caused a significant further increase in lesion area at both sites. EC-Abca1/g1 deficiency dramatically enhanced macrophage lipid accumulation in the branches of the aorta that are exposed to disturbed blood flow, decreased aortic endothelial NO synthase activity, and increased monocyte infiltration into the atherosclerotic plaque. Abca1/g1 deficiency enhanced lipopolysaccharide-induced inflammatory gene expression in mouse aortic ECs, which was recapitulated by ABCG1 deficiency in human aortic ECs.
conclusionsThese studies provide direct evidence that endothelial cholesterol efflux pathways mediated by ABCA1 and ABCG1 are nonredundant and atheroprotective, reflecting preservation of endothelial NO synthase activity and suppression of endothelial inflammation, especially in regions of disturbed arterial blood flow.
Indexed as
AnimalsAorta, ThoracicAortic DiseasesAtherosclerosisATP Binding Cassette Transporter 1ATP Binding Cassette Transporter, Subfamily G, Member 1Bone Marrow TransplantationCholesterolDiet, High-FatDisease Models, AnimalDisease ProgressionEndothelial CellsGenetic Predisposition to DiseaseInflammation MediatorsMacrophagesMaleAbca1 protein, mouseABCG1 protein, mouseATP Binding Cassette Transporter 1ATP Binding Cassette Transporter, Subfamily G, Member 1CholesterolInflammation MediatorsNitric Oxide Synthase Type IIINos3 protein, mouseReceptors, LDLatherosclerosisATP-binding cassette transportersendotheliumhypercholesterolemia
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