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John L. Dart Library
9 a.m. – 7 p.m.
Phone: (843) 722-7550
West Ashley Library
9 a.m. – 7 p.m.
Phone: (843) 766-6635
Folly Beach Library
Closed
Phone: (843) 588-2001
Edgar Allan Poe/Sullivan's Island Library
Closed for renovations
Phone: (843) 883-3914
Wando Mount Pleasant Library
9 a.m. – 8 p.m.
Phone: (843) 805-6888
Village Library
9 a.m. – 6 p.m.
Phone: (843) 884-9741
St. Paul's/Hollywood Library
9 a.m. – 8 p.m.
Phone: (843) 889-3300
Otranto Road Library
9 a.m. – 8 p.m.
Phone: (843) 572-4094
Mt. Pleasant Library
9 a.m. – 8 p.m.
Phone: (843) 849-6161
McClellanville Library
9 a.m. - 6 p.m.
Phone: (843) 887-3699
Keith Summey North Charleston Library
9 a.m. – 8 p.m.
Phone: (843) 744-2489
John's Island Library
9 a.m. – 8 p.m.
Phone: (843) 559-1945
Hurd/St. Andrews Library
9 a.m. – 8 p.m.
Phone: (843) 766-2546
Miss Jane's Building (Edisto Library Temporary Location)
9 a.m. – 6 p.m.
Phone: (843) 869-2355
Dorchester Road Library
9 a.m. – 8 p.m.
Phone: (843) 552-6466
Baxter-Patrick James Island
9 a.m. – 8 p.m.
Phone: (843) 795-6679
Main Library
9 a.m. – 8 p.m.
Phone: (843) 805-6930
Bees Ferry West Ashley Library
9 a.m. – 8 p.m.
Phone: (843) 805-6892
Mobile Library
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Phone: (843) 805-6909
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Functional investigation of the coronary artery disease gene SVEP1.
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- Author(s): Winkler, Michael J.; Müller, Philipp; Sharifi, Amin M.; Wobst, Jana; Winter, Hanna; Mokry, Michal; Ma, Lijiang; van der Laan, Sander W.; Pang, Shichao; Miritsch, Benedikt; Hinterdobler, Julia; Werner, Julia; Stiller, Barbara; Güldener, Ulrich; Webb, Tom R.; Asselbergs, Folkert W.; Björkegren, Johan L. M.; Maegdefessel, Lars; Schunkert, Heribert; Sager, Hendrik B.
- Source:
Basic Research in Cardiology; Dec2020, Vol. 115 Issue 6, p1-14, 14p - Source:
- Additional Information
- 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, 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. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Basic Research in Cardiology is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Abstract:
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