{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T13:17:38Z","timestamp":1791206258938,"version":"4.1.0"},"reference-count":51,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2014,11]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>Apoptosis of vascular smooth muscle cells (VSMCs) contributes to thinning and rupture of the atherosclerotic plaque fibrous cap and is thereby associated with myocardial infarction. Wnt protein activation of \u03b2-catenin regulates numerous genes that are associated with cell survival. We therefore investigated Wnt\/\u03b2-catenin survival signaling in VSMCs and assessed the presence of this pathway in human atherosclerotic plaques at various stages of the disease process.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results\u2014<\/jats:title>\n            <jats:p>\n              Wnt5a induced \u03b2-catenin\/T-cell factor signaling and retarded oxidative stress (H\n              <jats:sub>2<\/jats:sub>\n              O\n              <jats:sub>2<\/jats:sub>\n              )\u2013induced apoptosis in mouse aortic VSMCs. Quantification of mRNA levels revealed a &gt;4-fold (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05; n=9) increase in the expression of the Wnt\/\u03b2-catenin responsive gene, Wnt1-inducible secreted protein-1 (WISP-1), which was dependent on cAMP response element\u2013binding protein and sustained in the presence of H\n              <jats:sub>2<\/jats:sub>\n              O\n              <jats:sub>2<\/jats:sub>\n              . Exogenous WISP-1 significantly reduced H\n              <jats:sub>2<\/jats:sub>\n              O\n              <jats:sub>2<\/jats:sub>\n              \u2013induced apoptosis by 43% (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05; n=3) and was shown using silencing small interfering RNA, to be important for Wnt5a-dependent survival responses to H\n              <jats:sub>2<\/jats:sub>\n              O\n              <jats:sub>2<\/jats:sub>\n              (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05; n=3). WISP-1 protein levels were significantly lower (\u224850%) in unstable atherosclerosis compared with stable plaques (n=11 and n=14).\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>These results indicate for the first time that Wnt5a induces \u03b2-catenin survival signaling in VSMCs via WISP-1. The deficiency of the novel survival factor, WISP-1 in intimal VSMCs of unstable coronary plaques, suggests that there is altered Wnt\/\u03b2-catenin\/ T-cell factor signaling with progressive atherosclerosis, and restoration of WISP-1 protein might be an effective stabilization factor for vulnerable atherosclerotic plaques.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.114.303922","type":"journal-article","created":{"date-parts":[[2014,9,12]],"date-time":"2014-09-12T03:04:29Z","timestamp":1410491069000},"page":"2449-2456","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":41,"title":["Wnt5a-Induced Wnt1-Inducible Secreted Protein-1 Suppresses Vascular Smooth Muscle Cell Apoptosis Induced by Oxidative Stress"],"prefix":"10.1161","volume":"34","author":[{"given":"Carina","family":"Mill","sequence":"first","affiliation":[{"name":"From the School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bethan Alice","family":"Monk","sequence":"additional","affiliation":[{"name":"From the School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helen","family":"Williams","sequence":"additional","affiliation":[{"name":"From the School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven John","family":"Simmonds","sequence":"additional","affiliation":[{"name":"From the School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jamie Yancey","family":"Jeremy","sequence":"additional","affiliation":[{"name":"From the School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jason Lee","family":"Johnson","sequence":"additional","affiliation":[{"name":"From the School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah Jane","family":"George","sequence":"additional","affiliation":[{"name":"From the School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_5_2_2","doi-asserted-by":"publisher","DOI":"10.1097\/00041433-199510000-00013"},{"key":"e_1_3_5_3_2","doi-asserted-by":"publisher","DOI":"10.1136\/hrt.69.5.377"},{"key":"e_1_3_5_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.20.5.1262"},{"key":"e_1_3_5_5_2","doi-asserted-by":"publisher","DOI":"10.1007\/s10016-001-0331-1"},{"key":"e_1_3_5_6_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.atv.0000150649.39934.13"},{"key":"e_1_3_5_7_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.87.3.179"},{"key":"e_1_3_5_8_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.97.23.2307"},{"key":"e_1_3_5_9_2","first-page":"367","article-title":"Apoptosis is abundant in human atherosclerotic lesions, especially in inflammatory cells (macrophages and T cells), and may contribute to the accumulation of gruel and plaque instability.","volume":"149","author":"Bj\u00f6rkerud S","year":"1996","unstructured":"Bj\u00f6rkerud S, Bj\u00f6rkerud B. 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