{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T19:10:09Z","timestamp":1780081809189,"version":"3.54.0"},"reference-count":51,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2017,5]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>Smooth muscle cells (SMCs) contribute to neointima formation after vascular injury. Although \u03b2-catenin expression is induced after injury, whether its function is essential in SMCs for neointimal growth is unknown. Moreover, although inhibitors of \u03b2-catenin have been developed, their effects on SMC growth have not been tested. We assessed the requirement for SMC \u03b2-catenin in short-term vascular homeostasis and in response to arterial injury and investigated the effects of \u03b2-catenin inhibitors on vascular SMC growth.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results\u2014<\/jats:title>\n            <jats:p>\n              We used an inducible, conditional genetic deletion of \u03b2-catenin in SMCs of adult mice. Uninjured arteries from adult mice lacking SMC \u03b2-catenin were indistinguishable from controls in terms of structure and SMC marker gene expression. After carotid artery ligation, however, vessels from mice lacking SMC \u03b2-catenin developed smaller neointimas, with lower neointimal cell proliferation and increased apoptosis. SMCs lacking \u03b2-catenin showed decreased mRNA expression of\n              <jats:italic>Mmp2<\/jats:italic>\n              ,\n              <jats:italic>Mmp9<\/jats:italic>\n              ,\n              <jats:italic>Sphk1<\/jats:italic>\n              , and\n              <jats:italic>S1pr1<\/jats:italic>\n              (genes that promote neointima formation), higher levels of\n              <jats:italic>Jag1<\/jats:italic>\n              and\n              <jats:italic>Gja1<\/jats:italic>\n              (genes that inhibit neointima formation), decreased Mmp2 protein expression and secretion, and reduced cell invasion in vitro. Moreover, \u03b2-catenin inhibitors PKF118-310 and ICG-001 limited growth of mouse and human vascular SMCs in a dose-dependent manner.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>SMC \u03b2-catenin is dispensable for maintenance of the structure and state of differentiation of uninjured adult arteries, but is required for neointima formation after vascular injury. Pharmacological \u03b2-catenin inhibitors hinder growth of human vascular SMCs. Thus, inhibiting \u03b2-catenin has potential as a therapy to limit SMC accumulation and vascular obstruction.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.116.308643","type":"journal-article","created":{"date-parts":[[2017,3,17]],"date-time":"2017-03-17T01:10:36Z","timestamp":1489713036000},"page":"879-888","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":24,"title":["Inhibition of Smooth Muscle \u03b2-Catenin Hinders Neointima Formation After Vascular Injury"],"prefix":"10.1161","volume":"37","author":[{"given":"Dario F.","family":"Riascos-Bernal","sequence":"first","affiliation":[{"name":"From the Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), and Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY (D.F.R.-B., P.C., J.N.G., V.A., L.E.-G., D.P., S.J., N.E.S.S.); and CVPath Institute, Gaithersburg, MD (L.G.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Prameladevi","family":"Chinnasamy","sequence":"additional","affiliation":[{"name":"From the Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), and Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY (D.F.R.-B., P.C., J.N.G., V.A., L.E.-G., D.P., S.J., N.E.S.S.); and CVPath Institute, Gaithersburg, MD (L.G.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jordana N.","family":"Gross","sequence":"additional","affiliation":[{"name":"From the Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), and Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY (D.F.R.-B., P.C., J.N.G., V.A., L.E.-G., D.P., S.J., N.E.S.S.); and CVPath Institute, Gaithersburg, MD (L.G.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vanessa","family":"Almonte","sequence":"additional","affiliation":[{"name":"From the Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), and Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY (D.F.R.-B., P.C., J.N.G., V.A., L.E.-G., D.P., S.J., N.E.S.S.); and CVPath Institute, Gaithersburg, MD (L.G.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lander","family":"Ega\u00f1a-Gorro\u00f1o","sequence":"additional","affiliation":[{"name":"From the Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), and Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY (D.F.R.-B., P.C., J.N.G., V.A., L.E.-G., D.P., S.J., N.E.S.S.); and CVPath Institute, Gaithersburg, MD (L.G.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dippal","family":"Parikh","sequence":"additional","affiliation":[{"name":"From the Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), and Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY (D.F.R.-B., P.C., J.N.G., V.A., L.E.-G., D.P., S.J., N.E.S.S.); and CVPath Institute, Gaithersburg, MD (L.G.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Smitha","family":"Jayakumar","sequence":"additional","affiliation":[{"name":"From the Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), and Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY (D.F.R.-B., P.C., J.N.G., V.A., L.E.-G., D.P., S.J., N.E.S.S.); and CVPath Institute, Gaithersburg, MD 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