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Title: | Monocyte adhesion to atherosclerotic matrix proteins is enhanced by Asn-Gly-Arg deamidation | Authors: | Dutta, Bamaprasad Park, Jung Eun Kumar, Subodh Hao, Piliang Gallart-Palau, Xavier Serra, Aida Ren, Yan Sorokin, Vitaly Lee, Chuen Neng Ho, Hee Hwa de Kleijn, Dominique Sze, Siu Kwan |
Keywords: | DRNTU::Science::Biological sciences Protein Deamidation Monocyte Adhesion |
Issue Date: | 2017 | Source: | Dutta, B., Park, J. E., Kumar, S., Hao, P., Gallart-Palau, X., Serra, A., . . . Sze, S. K. (2017). Monocyte adhesion to atherosclerotic matrix proteins is enhanced by Asn-Gly-Arg deamidation. Scientific Reports, 7, 5765-. doi:10.1038/s41598-017-06202-2 | Series/Report no.: | Scientific Reports | Abstract: | Atherosclerosis arises from leukocyte infiltration and thickening of the artery walls and constitutes a major component of vascular disease pathology, but the molecular events underpinning this process are not fully understood. Proteins containing an Asn-Gly-Arg (NGR) motif readily undergo deamidation of asparagine to generate isoDGR structures that bind to integrin αvβ3 on circulating leukocytes. Here we report the identification of isoDGR motifs in human atherosclerotic plaque components including extracellular matrix (ECM) proteins fibronectin and tenascin C, which have been strongly implicated in human atherosclerosis. We further demonstrate that deamidation of NGR motifs in fibronectin and tenascin C leads to increased adhesion of the monocytic cell line U937 and enhanced binding of primary human monocytes, except in the presence of a αvβ3-blocking antibody or the αv-selective inhibitor cilengitide. In contrast, under the same deamidating conditions monocyte-macrophages displayed only weak binding to the alternative ECM component vitronectin which lacks NGR motifs. Together, these findings confirm a critical role for isoDGR motifs in mediating leukocyte adhesion to the ECM via integrin αvβ3 and suggest that protein deamidation may promote the pathological progression of human atherosclerosis by enhancing monocyte recruitment to developing plaques. | URI: | https://hdl.handle.net/10356/88130 http://hdl.handle.net/10220/45631 |
ISSN: | 2045-2322 | DOI: | 10.1038/s41598-017-06202-2 | Rights: | © 2017 The Author(s). This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/. | Fulltext Permission: | open | Fulltext Availability: | With Fulltext |
Appears in Collections: | SBS Journal Articles |
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