{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T02:06:38Z","timestamp":1778637998742,"version":"3.51.4"},"reference-count":38,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2016,9]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>The chronic inflammation associated with atherosclerosis is caused by lipid deposition followed by leukocyte recruitment to the arterial wall. We previously showed that the hematopoietic cell\u2013specific adaptor protein Cas- and Hef1-associated signal transducer hematopoietic isoform (Chat-H)\/SHEP1 regulated lymphocyte adhesion and migration. In this study, we analyzed the role of Chat-H in atherosclerosis development.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results\u2014<\/jats:title>\n            <jats:p>\n              Using Chat-H\u2013deficient bone marrow transplantation in low-density lipoprotein receptor\u2013deficient mice, we found that Chat-H regulated atherosclerotic plaque formation. Chat-H deficiency in hematopoietic cells associated with lower plaque complexity and fewer leukocytes in the lesions, whereas myeloid-specific deletion of Chat-H was sufficient for conferring atheroprotection. Chat-H deficiency resulted in reduced recruitment of classical Ly6c\n              <jats:sup>high<\/jats:sup>\n              and nonclassical Ly6c\n              <jats:sup>low<\/jats:sup>\n              monocytes to the plaques, which was accompanied by increased numbers of both monocyte subsets in the blood. This associated with defective adhesion of Chat-H\u2013deficient Ly6c\n              <jats:sup>high<\/jats:sup>\n              and Ly6c\n              <jats:sup>low<\/jats:sup>\n              monocytes to vascular cell adhesion molecule-1 in vitro and impaired infiltration of fluorescent bead\u2013loaded monocytes to atherosclerotic plaques. In contrast, Chat-H was dispensable for CX3CL1 and CCR1\/CCR5-dependent migration of monocytes.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>Our findings highlight Chat-H as a key protein that regulates atherosclerosis development by controlling monocyte adhesion and recruitment to the plaques and identify a novel target that may be exploited for treating atherosclerosis.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.116.308014","type":"journal-article","created":{"date-parts":[[2016,7,15]],"date-time":"2016-07-15T03:14:36Z","timestamp":1468552476000},"page":"1791-1801","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":30,"title":["Monocyte Adhesion and Plaque Recruitment During Atherosclerosis Development Is Regulated by the Adapter Protein Chat-H\/SHEP1"],"prefix":"10.1161","volume":"36","author":[{"given":"Olivier","family":"Herbin","sequence":"first","affiliation":[{"name":"From the Icahn School of Medicine at Mount Sinai, Department of Medicine, The Immunology Institute, New York (O.H., E.G.W., K.A.); Quartzy, Inc, Palo Alto, CA (A.G.R.); and Leon H. Charney Division of Cardiology, Department of Medicine, NYU School of Medicine, New York (B.R., K.J.M.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Adam G.","family":"Regelmann","sequence":"additional","affiliation":[{"name":"From the Icahn School of Medicine at Mount Sinai, Department of Medicine, The Immunology Institute, New York (O.H., E.G.W., K.A.); Quartzy, Inc, Palo Alto, CA (A.G.R.); and Leon H. Charney Division of Cardiology, Department of Medicine, NYU School of Medicine, New York (B.R., K.J.M.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bhama","family":"Ramkhelawon","sequence":"additional","affiliation":[{"name":"From the Icahn School of Medicine at Mount Sinai, Department of Medicine, The Immunology Institute, New York (O.H., E.G.W., K.A.); Quartzy, Inc, Palo Alto, CA (A.G.R.); and Leon H. Charney Division of Cardiology, Department of Medicine, NYU School of Medicine, New York (B.R., K.J.M.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Erica G.","family":"Weinstein","sequence":"additional","affiliation":[{"name":"From the Icahn School of Medicine at Mount Sinai, Department of Medicine, The Immunology Institute, New York (O.H., E.G.W., K.A.); Quartzy, Inc, Palo Alto, CA (A.G.R.); and Leon H. Charney Division of Cardiology, Department of Medicine, NYU School of Medicine, New York (B.R., K.J.M.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kathryn J.","family":"Moore","sequence":"additional","affiliation":[{"name":"From the Icahn School of Medicine at Mount Sinai, Department of Medicine, The Immunology Institute, New York (O.H., E.G.W., K.A.); Quartzy, Inc, Palo Alto, CA (A.G.R.); and Leon H. Charney Division of Cardiology, Department of Medicine, NYU School of Medicine, New York (B.R., K.J.M.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Konstantina","family":"Alexandropoulos","sequence":"additional","affiliation":[{"name":"From the Icahn School of Medicine at Mount Sinai, Department of Medicine, The Immunology Institute, New York (O.H., E.G.W., K.A.); Quartzy, Inc, Palo Alto, CA (A.G.R.); and Leon H. 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