Functional investigation of the coronary artery disease gene SVEP1
A missense variant of the sushi, von Willebrand factor type A, EGF and pentraxin domain containing protein 1 (SVEP1) is genome-wide significantly associated with coronary artery disease. The mechanisms how SVEP1 impacts atherosclerosis are not known. We found endothelial cells (EC) and vascular smoo...
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| Published in | Basic research in cardiology Vol. 115; no. 6; p. 67 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.12.2020
Springer Nature B.V |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0300-8428 1435-1803 1435-1803 |
| DOI | 10.1007/s00395-020-00828-6 |
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| Abstract | A missense variant of the sushi, von Willebrand factor type A, EGF and pentraxin domain containing protein 1 (SVEP1) is genome-wide significantly associated with coronary artery disease. The mechanisms how SVEP1 impacts atherosclerosis are not known. We found endothelial cells (EC) and vascular smooth muscle cells to represent the major cellular source of SVEP1 in plaques. Plaques were larger in atherosclerosis-prone Svep1 haploinsufficient (
ApoE
−/−
Svep1
+/−
) compared to Svep1 wild-type mice
(ApoE
−/−
Svep1
+/+
) and
ApoE
−/−
Svep1
+/−
mice displayed elevated plaque neutrophil, Ly6C
high
monocyte, and macrophage numbers. We assessed how leukocytes accumulated more inside plaques in
ApoE
−/−
Svep1
+/−
mice and found enhanced leukocyte recruitment from blood into plaques. In vitro, we examined how SVEP1 deficiency promotes leukocyte recruitment and found elevated expression of the leukocyte attractant chemokine (C-X-C motif) ligand 1 (
CXCL1
) in EC after incubation with missense compared to wild-type SVEP1. Increasing wild-type SVEP1 levels silenced endothelial CXCL1 release. In line, plasma Cxcl1 levels were elevated in
ApoE
−/−
Svep1
+/−
mice. Our studies reveal an atheroprotective role of SVEP1. Deficiency of wild-type Svep1 increased endothelial
CXCL1
expression leading to enhanced recruitment of proinflammatory leukocytes from blood to plaque. Consequently, elevated vascular inflammation resulted in enhanced plaque progression in Svep1 deficiency. |
|---|---|
| AbstractList | A missense variant of the sushi, von Willebrand factor type A, EGF and pentraxin domain containing protein 1 (SVEP1) is genome-wide significantly associated with coronary artery disease. The mechanisms how SVEP1 impacts atherosclerosis are not known. We found endothelial cells (EC) and vascular smooth muscle cells to represent the major cellular source of SVEP1 in plaques. Plaques were larger in atherosclerosis-prone Svep1 haploinsufficient (ApoE−/−Svep1+/−) compared to Svep1 wild-type mice (ApoE−/−Svep1+/+) and ApoE−/−Svep1+/− mice displayed elevated plaque neutrophil, Ly6Chigh monocyte, and macrophage numbers. We assessed how leukocytes accumulated more inside plaques in ApoE−/−Svep1+/− mice and found enhanced leukocyte recruitment from blood into plaques. In vitro, we examined how SVEP1 deficiency promotes leukocyte recruitment and found elevated expression of the leukocyte attractant chemokine (C-X-C motif) ligand 1 (CXCL1) in EC after incubation with missense compared to wild-type SVEP1. Increasing wild-type SVEP1 levels silenced endothelial CXCL1 release. In line, plasma Cxcl1 levels were elevated in ApoE−/−Svep1+/− mice. Our studies reveal an atheroprotective role of SVEP1. Deficiency of wild-type Svep1 increased endothelial CXCL1 expression leading to enhanced recruitment of proinflammatory leukocytes from blood to plaque. Consequently, elevated vascular inflammation resulted in enhanced plaque progression in Svep1 deficiency. A missense variant of the sushi, von Willebrand factor type A, EGF and pentraxin domain containing protein 1 (SVEP1) is genome-wide significantly associated with coronary artery disease. The mechanisms how SVEP1 impacts atherosclerosis are not known. We found endothelial cells (EC) and vascular smooth muscle cells to represent the major cellular source of SVEP1 in plaques. Plaques were larger in atherosclerosis-prone Svep1 haploinsufficient ( ApoE −/− Svep1 +/− ) compared to Svep1 wild-type mice (ApoE −/− Svep1 +/+ ) and ApoE −/− Svep1 +/− mice displayed elevated plaque neutrophil, Ly6C high monocyte, and macrophage numbers. We assessed how leukocytes accumulated more inside plaques in ApoE −/− Svep1 +/− mice and found enhanced leukocyte recruitment from blood into plaques. In vitro, we examined how SVEP1 deficiency promotes leukocyte recruitment and found elevated expression of the leukocyte attractant chemokine (C-X-C motif) ligand 1 ( CXCL1 ) in EC after incubation with missense compared to wild-type SVEP1. Increasing wild-type SVEP1 levels silenced endothelial CXCL1 release. In line, plasma Cxcl1 levels were elevated in ApoE −/− Svep1 +/− mice. Our studies reveal an atheroprotective role of SVEP1. Deficiency of wild-type Svep1 increased endothelial CXCL1 expression leading to enhanced recruitment of proinflammatory leukocytes from blood to plaque. Consequently, elevated vascular inflammation resulted in enhanced plaque progression in Svep1 deficiency. A missense variant of the sushi, von Willebrand factor type A, EGF and pentraxin domain containing protein 1 (SVEP1) is genome-wide significantly associated with coronary artery disease. The mechanisms how SVEP1 impacts atherosclerosis are not known. We found endothelial cells (EC) and vascular smooth muscle cells to represent the major cellular source of SVEP1 in plaques. Plaques were larger in atherosclerosis-prone Svep1 haploinsufficient (ApoE Svep1 ) compared to Svep1 wild-type mice (ApoE Svep1 ) and ApoE Svep1 mice displayed elevated plaque neutrophil, Ly6C monocyte, and macrophage numbers. We assessed how leukocytes accumulated more inside plaques in ApoE Svep1 mice and found enhanced leukocyte recruitment from blood into plaques. In vitro, we examined how SVEP1 deficiency promotes leukocyte recruitment and found elevated expression of the leukocyte attractant chemokine (C-X-C motif) ligand 1 (CXCL1) in EC after incubation with missense compared to wild-type SVEP1. Increasing wild-type SVEP1 levels silenced endothelial CXCL1 release. In line, plasma Cxcl1 levels were elevated in ApoE Svep1 mice. Our studies reveal an atheroprotective role of SVEP1. Deficiency of wild-type Svep1 increased endothelial CXCL1 expression leading to enhanced recruitment of proinflammatory leukocytes from blood to plaque. Consequently, elevated vascular inflammation resulted in enhanced plaque progression in Svep1 deficiency. A missense variant of the sushi, von Willebrand factor type A, EGF and pentraxin domain containing protein 1 (SVEP1) is genome-wide significantly associated with coronary artery disease. The mechanisms how SVEP1 impacts atherosclerosis are not known. We found endothelial cells (EC) and vascular smooth muscle cells to represent the major cellular source of SVEP1 in plaques. Plaques were larger in atherosclerosis-prone Svep1 haploinsufficient (ApoE-/-Svep1+/-) compared to Svep1 wild-type mice (ApoE-/-Svep1+/+) and ApoE-/-Svep1+/- mice displayed elevated plaque neutrophil, Ly6Chigh monocyte, and macrophage numbers. We assessed how leukocytes accumulated more inside plaques in ApoE-/-Svep1+/- mice and found enhanced leukocyte recruitment from blood into plaques. In vitro, we examined how SVEP1 deficiency promotes leukocyte recruitment and found elevated expression of the leukocyte attractant chemokine (C-X-C motif) ligand 1 (CXCL1) in EC after incubation with missense compared to wild-type SVEP1. Increasing wild-type SVEP1 levels silenced endothelial CXCL1 release. In line, plasma Cxcl1 levels were elevated in ApoE-/-Svep1+/- mice. Our studies reveal an atheroprotective role of SVEP1. Deficiency of wild-type Svep1 increased endothelial CXCL1 expression leading to enhanced recruitment of proinflammatory leukocytes from blood to plaque. Consequently, elevated vascular inflammation resulted in enhanced plaque progression in Svep1 deficiency.A missense variant of the sushi, von Willebrand factor type A, EGF and pentraxin domain containing protein 1 (SVEP1) is genome-wide significantly associated with coronary artery disease. The mechanisms how SVEP1 impacts atherosclerosis are not known. We found endothelial cells (EC) and vascular smooth muscle cells to represent the major cellular source of SVEP1 in plaques. Plaques were larger in atherosclerosis-prone Svep1 haploinsufficient (ApoE-/-Svep1+/-) compared to Svep1 wild-type mice (ApoE-/-Svep1+/+) and ApoE-/-Svep1+/- mice displayed elevated plaque neutrophil, Ly6Chigh monocyte, and macrophage numbers. We assessed how leukocytes accumulated more inside plaques in ApoE-/-Svep1+/- mice and found enhanced leukocyte recruitment from blood into plaques. In vitro, we examined how SVEP1 deficiency promotes leukocyte recruitment and found elevated expression of the leukocyte attractant chemokine (C-X-C motif) ligand 1 (CXCL1) in EC after incubation with missense compared to wild-type SVEP1. Increasing wild-type SVEP1 levels silenced endothelial CXCL1 release. In line, plasma Cxcl1 levels were elevated in ApoE-/-Svep1+/- mice. Our studies reveal an atheroprotective role of SVEP1. Deficiency of wild-type Svep1 increased endothelial CXCL1 expression leading to enhanced recruitment of proinflammatory leukocytes from blood to plaque. Consequently, elevated vascular inflammation resulted in enhanced plaque progression in Svep1 deficiency. |
| ArticleNumber | 67 |
| Author | Kessler, Thorsten Ma, Lijiang Webb, Tom R. Pang, Shichao Güldener, Ulrich Winter, Hanna Miritsch, Benedikt Schunkert, Heribert Hinterdobler, Julia Stiller, Barbara Werner, Julia Asselbergs, Folkert W. Wobst, Jana van der Laan, Sander W. Sager, Hendrik B. Sharifi, Amin M. Björkegren, Johan L. M. Müller, Philipp Mokry, Michal Winkler, Michael J. Maegdefessel, Lars |
| Author_xml | – sequence: 1 givenname: Michael J. surname: Winkler fullname: Winkler, Michael J. organization: Department of Cardiology, German Heart Centre Munich, Technical University of Munich, German Centre for Cardiovascular Research (DZHK e.V.), Partner Site Munich Heart Alliance – sequence: 2 givenname: Philipp surname: Müller fullname: Müller, Philipp organization: Department of Cardiology, German Heart Centre Munich, Technical University of Munich, German Centre for Cardiovascular Research (DZHK e.V.), Partner Site Munich Heart Alliance – sequence: 3 givenname: Amin M. surname: Sharifi fullname: Sharifi, Amin M. organization: Department of Cardiology, German Heart Centre Munich, Technical University of Munich, German Centre for Cardiovascular Research (DZHK e.V.), Partner Site Munich Heart Alliance – sequence: 4 givenname: Jana surname: Wobst fullname: Wobst, Jana organization: Department of Cardiology, German Heart Centre Munich, Technical University of Munich, German Centre for Cardiovascular Research (DZHK e.V.), Partner Site Munich Heart Alliance – sequence: 5 givenname: Hanna surname: Winter fullname: Winter, Hanna organization: German Centre for Cardiovascular Research (DZHK e.V.), Partner Site Munich Heart Alliance, Vascular Biology and Experimental Vascular Medicine Unit, Department of Vascular and Endovascular Surgery, Klinikum rechts der Isar, Technical University Munich – sequence: 6 givenname: Michal surname: Mokry fullname: Mokry, Michal organization: Division of Heart and Lungs, Department of Cardiology, University Medical Center Utrecht – sequence: 7 givenname: Lijiang surname: Ma fullname: Ma, Lijiang organization: Department of Genetics and Genomic Sciences, Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai – sequence: 8 givenname: Sander W. surname: van der Laan fullname: van der Laan, Sander W. organization: Division of Heart and Lungs, Department of Cardiology, University Medical Center Utrecht – sequence: 9 givenname: Shichao surname: Pang fullname: Pang, Shichao organization: Department of Cardiology, German Heart Centre Munich, Technical University of Munich – sequence: 10 givenname: Benedikt surname: Miritsch fullname: Miritsch, Benedikt organization: Department of Cardiology, German Heart Centre Munich, Technical University of Munich, German Centre for Cardiovascular Research (DZHK e.V.), Partner Site Munich Heart Alliance – sequence: 11 givenname: Julia surname: Hinterdobler fullname: Hinterdobler, Julia organization: Department of Cardiology, German Heart Centre Munich, Technical University of Munich, German Centre for Cardiovascular Research (DZHK e.V.), Partner Site Munich Heart Alliance – sequence: 12 givenname: Julia surname: Werner fullname: Werner, Julia organization: Department of Cardiology, German Heart Centre Munich, Technical University of Munich, German Centre for Cardiovascular Research (DZHK e.V.), Partner Site Munich Heart Alliance – sequence: 13 givenname: Barbara surname: Stiller fullname: Stiller, Barbara organization: Department of Cardiology, German Heart Centre Munich, Technical University of Munich – sequence: 14 givenname: Ulrich surname: Güldener fullname: Güldener, Ulrich organization: Department of Cardiology, German Heart Centre Munich, Technical University of Munich – sequence: 15 givenname: Tom R. surname: Webb fullname: Webb, Tom R. organization: Department of Cardiovascular Sciences, University of Leicester, and National Institute for Health Research (NIHR) Leicester Cardiovascular Biomedical Research Centre – sequence: 16 givenname: Folkert W. surname: Asselbergs fullname: Asselbergs, Folkert W. organization: Division of Heart and Lungs, Department of Cardiology, University Medical Center Utrecht, Institute of Cardiovascular Science, Faculty of Population Health Sciences, and Health Data Research UK and Institute of Health Informatics, University College London – sequence: 17 givenname: Johan L. M. surname: Björkegren fullname: Björkegren, Johan L. M. organization: Department of Genetics and Genomic Sciences, Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, Integrated Cardio Metabolic Centre, Department of Medicine, Karolinska Institutet, Karolinska Universitetssjukhuset, Department of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu – sequence: 18 givenname: Lars surname: Maegdefessel fullname: Maegdefessel, Lars organization: German Centre for Cardiovascular Research (DZHK e.V.), Partner Site Munich Heart Alliance, Vascular Biology and Experimental Vascular Medicine Unit, Department of Vascular and Endovascular Surgery, Klinikum rechts der Isar, Technical University Munich – sequence: 19 givenname: Heribert surname: Schunkert fullname: Schunkert, Heribert organization: Department of Cardiology, German Heart Centre Munich, Technical University of Munich, German Centre for Cardiovascular Research (DZHK e.V.), Partner Site Munich Heart Alliance – sequence: 20 givenname: Hendrik B. surname: Sager fullname: Sager, Hendrik B. email: hendrik.sager@tum.de organization: Department of Cardiology, German Heart Centre Munich, Technical University of Munich, German Centre for Cardiovascular Research (DZHK e.V.), Partner Site Munich Heart Alliance – sequence: 21 givenname: Thorsten orcidid: 0000-0003-3326-1621 surname: Kessler fullname: Kessler, Thorsten email: thorsten.kessler@tum.de organization: Department of Cardiology, German Heart Centre Munich, Technical University of Munich, German Centre for Cardiovascular Research (DZHK e.V.), Partner Site Munich Heart Alliance |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33185739$$D View this record in MEDLINE/PubMed http://kipublications.ki.se/Default.aspx?queryparsed=id:145338697$$DView record from Swedish Publication Index |
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| ContentType | Journal Article |
| Copyright | The Author(s) 2020 The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
| Copyright_xml | – notice: The Author(s) 2020 – notice: The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| DOI | 10.1007/s00395-020-00828-6 |
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| Issue | 6 |
| Keywords | Genetics SVEP1 Coronary artery disease Atherosclerosis |
| Language | English |
| License | Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
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| PublicationTitle | Basic research in cardiology |
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| Snippet | A missense variant of the sushi, von Willebrand factor type A, EGF and pentraxin domain containing protein 1 (SVEP1) is genome-wide significantly associated... |
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| SubjectTerms | Animals Antigens, Ly - metabolism Apolipoprotein E Arteriosclerosis Atherosclerosis Blood Calcium-Binding Proteins - deficiency Calcium-Binding Proteins - genetics Calcium-Binding Proteins - metabolism Cardiology Cardiovascular disease Cell Adhesion Molecules - deficiency Cell Adhesion Molecules - genetics Cell Adhesion Molecules - metabolism Cells, Cultured Chemokine CXCL1 - genetics Chemokine CXCL1 - metabolism Chemokines Chemotaxis, Leukocyte Coronary artery Coronary artery disease Coronary Artery Disease - genetics Coronary Artery Disease - metabolism Coronary Artery Disease - pathology Coronary vessels Coronary Vessels - metabolism Coronary Vessels - pathology Disease Models, Animal Endothelial cells Endothelial Cells - metabolism Endothelial Cells - pathology Genetic Association Studies Genetic Predisposition to Disease Genomes Haploinsufficiency Heart diseases Humans Inflammation Leukocyte migration Leukocytes Macrophages Macrophages - metabolism Medicine Medicine & Public Health Mice, Inbred C57BL Mice, Knockout, ApoE Monocytes Muscles Myocytes, Smooth Muscle - metabolism Myocytes, Smooth Muscle - pathology Neutrophil Infiltration Neutrophils - pathology Original Contribution Pentraxins Plaque, Atherosclerotic Plaques Polymorphism, Single Nucleotide Proteins - genetics Proteins - metabolism Recruitment Smooth muscle Von Willebrand factor |
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| Title | Functional investigation of the coronary artery disease gene SVEP1 |
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