{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T14:21:10Z","timestamp":1791037270122,"version":"4.1.0"},"reference-count":45,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2011,2,15]]},"abstract":"<jats:sec>\n            <jats:title>Background\u2014<\/jats:title>\n            <jats:p>\n              Microsomal (m) prostaglandin (PG) E\n              <jats:sub>2<\/jats:sub>\n              synthase (S)-1 catalyzes the formation of PGE\n              <jats:sub>2<\/jats:sub>\n              from PGH\n              <jats:sub>2<\/jats:sub>\n              , a cyclooxygenase product that is derived from arachidonic acid. Previous studies in mice suggest that targeting mPGES-1 may be less likely to cause hypertension or thrombosis than cyclooxygenase-2\u2013selective inhibition or deletion in vivo. Indeed, deletion of mPGES-1 retards atherogenesis and angiotensin II\u2013induced aortic aneurysm formation. The role of mPGES-1 in the response to vascular injury is unknown.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods and Results\u2014<\/jats:title>\n            <jats:p>\n              Mice were subjected to wire injury of the femoral artery. Both neointimal area and vascular stenosis were significantly reduced 4 weeks after injury in mPGES-1 knockout mice compared with wild-type controls (65.6\u00b15.7 versus 37.7\u00b15.1\u00d710\n              <jats:sup>3<\/jats:sup>\n              pixel area and 70.5\u00b113.4% versus 47.7\u00b117.4%, respectively;\n              <jats:italic>P<\/jats:italic>\n              &lt;0.01). Induction of tenascin-C, a proproliferative and promigratory extracellular matrix protein, after injury was attenuated in the knockouts. Consistent with in vivo rediversion of PG biosynthesis, mPGES-1\u2013deleted vascular smooth muscle cells generated less PGE\n              <jats:sub>2<\/jats:sub>\n              but more PGI\n              <jats:sub>2<\/jats:sub>\n              and expressed reduced tenascin-C compared with wild-type cells. Both suppression of PGE\n              <jats:sub>2<\/jats:sub>\n              and augmentation of PGI\n              <jats:sub>2<\/jats:sub>\n              attenuate tenascin-C expression and vascular smooth muscle cell proliferation and migration in vitro.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>Deletion of mPGES-1 in mice attenuates neointimal hyperplasia after vascular injury, in part by regulating tenascin-C expression. This raises for consideration the therapeutic potential of mPGES-1 inhibitors as adjuvant therapy for percutaneous coronary intervention.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circulationaha.110.973685","type":"journal-article","created":{"date-parts":[[2011,2,1]],"date-time":"2011-02-01T01:52:49Z","timestamp":1296525169000},"page":"631-639","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":87,"title":["Microsomal Prostaglandin E\n            <sub>2<\/sub>\n            Synthase-1 Modulates the Response to Vascular Injury"],"prefix":"10.1161","volume":"123","author":[{"given":"Miao","family":"Wang","sequence":"first","affiliation":[{"name":"From the Institute for Translational Medicine and Therapeutics (M.W., D.K., Z.Y., L.C., Y.C., J.A.L., R.K.A., G.A.G., K.I.-S., G.G., P.L.J.), Department of Pharmacology (M.W., D.K., Z.Y., L.C., Y.C., J.A.L., R.K.A., G.A.G.), and Institute for Medicine and Engineering (K.I.-S., M.C.T., P.L.J), Department of Pathology and Laboratory Medicine (K.I.-S., G.G., P.L.J.), University of Pennsylvania, Philadelphia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaori","family":"Ihida-Stansbury","sequence":"additional","affiliation":[{"name":"From the Institute for Translational Medicine and Therapeutics (M.W., D.K., Z.Y., L.C., Y.C., J.A.L., R.K.A., G.A.G., K.I.-S., G.G., P.L.J.), Department of Pharmacology (M.W., D.K., Z.Y., L.C., Y.C., J.A.L., R.K.A., G.A.G.), and Institute for Medicine and Engineering (K.I.-S., M.C.T., P.L.J), Department of Pathology and Laboratory Medicine (K.I.-S., G.G., P.L.J.), University of Pennsylvania, Philadelphia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Devashish","family":"Kothapalli","sequence":"additional","affiliation":[{"name":"From the Institute for Translational Medicine and Therapeutics (M.W., D.K., Z.Y., L.C., Y.C., J.A.L., R.K.A., G.A.G., K.I.-S., G.G., P.L.J.), Department of Pharmacology (M.W., D.K., Z.Y., L.C., Y.C., J.A.L., R.K.A., G.A.G.), and Institute for Medicine and Engineering (K.I.-S., M.C.T., P.L.J), Department of Pathology and Laboratory Medicine (K.I.-S., G.G., P.L.J.), University of Pennsylvania, Philadelphia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mathieu C.","family":"Tamby","sequence":"additional","affiliation":[{"name":"From the Institute for Translational Medicine and Therapeutics (M.W., D.K., Z.Y., L.C., Y.C., J.A.L., R.K.A., G.A.G., K.I.-S., G.G., P.L.J.), Department of Pharmacology (M.W., D.K., Z.Y., L.C., Y.C., J.A.L., R.K.A., G.A.G.), and Institute for Medicine and Engineering (K.I.-S., M.C.T., P.L.J), Department of Pathology and Laboratory Medicine (K.I.-S., G.G., P.L.J.), University of Pennsylvania, Philadelphia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhou","family":"Yu","sequence":"additional","affiliation":[{"name":"From the Institute for Translational Medicine and Therapeutics 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