{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,3]],"date-time":"2025-11-03T04:38:06Z","timestamp":1762144686678,"version":"3.37.0"},"reference-count":53,"publisher":"Portland Press Ltd.","issue":"9","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2010,5,1]]},"abstract":"<jats:p>In the present study, we tested the hypothesis that the PPAR\u03b3 (peroxisome-proliferator-activated receptor \u03b3) activator rosiglitazone improves vascular structure and function in aged hyperhomocysteinaemic MTHFR (methylene tetrahydrofolate reductase) gene heterozygous knockout (mthfr+\/\u2212) mice fed a HCD (high-cholesterol diet), a model of high cardiovascular risk. One-year-old mthfr+\/\u2212 mice were fed or not HCD (6\u00a0mg\u00b7kg\u22121 of body weight\u00b7day\u22121) and treated or not with rosiglitazone (20\u00a0mg\u00b7kg\u22121 of body weight\u00b7day\u22121) for 90\u00a0days and compared with wild-type mice. Endothelium-dependent relaxation of carotid arteries was significantly impaired (\u221240%) only in rosiglitazone-treated HCD-fed mthfr+\/\u2212 mice. Carotid M\/L (media-to-lumen ratio) and CSA (cross-sectional area) were increased (2-fold) in mthfr+\/\u2212 mice fed or not HCD compared with wild-type mice (P&amp;lt;0.05). Rosiglitazone reduced M\/L and CSA only in mthfr+\/\u2212 mice fed a normal diet. Superoxide production was increased in mthfr+\/\u2212 mice fed HCD treated or not with rosiglitazone, whereas plasma nitrite was decreased by rosiglitazone in mice fed or not HCD. PRMT-1 (protein arginine methyltransferase-1), involved in synthesis of the NO (nitric oxide) synthase inhibitor ADMA (asymmetric \u03c9-NG,NG-dimethylarginine), and ADMA were increased only in rosiglitazone-treated HCD-fed mthfr+\/\u2212 mice. Rosiglitazone had both beneficial and deleterious vascular effects in this animal model of high cardiovascular risk: it prevented carotid remodelling, but impaired endothelial function in part through enhanced oxidative stress and increased ADMA production in mice at high cardiovascular risk.<\/jats:p>","DOI":"10.1042\/cs20090289","type":"journal-article","created":{"date-parts":[[2009,12,10]],"date-time":"2009-12-10T14:00:37Z","timestamp":1260453637000},"page":"583-592","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Countervailing vascular effects of rosiglitazone in high cardiovascular risk mice: role of oxidative stress and PRMT-1"],"prefix":"10.1042","volume":"118","author":[{"given":"Carmine","family":"Savoia","sequence":"first","affiliation":[{"name":"Lady Davis Institute for Medical Research, Sir Mortimer B. 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