{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T21:25:55Z","timestamp":1790112355965,"version":"4.0.1"},"reference-count":64,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":2585,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2002,1]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>The role of smooth muscle\u2010derived lipoprotein lipase (LPL) that translocates to the endothelium surface on vascular dysfunction during atherogenesis is unclear. Thus, the role of vascular LPL on blood vessel reactivity was assessed in transgenic mice that specifically express human LPL in the circulatory system.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Aortic free fatty acids (FFAs) were increased by 69% in the transgenic mice expressing human LPL in aortic smooth muscle cells (L2LPL) compared with their non\u2010transgenic littermates (L2).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Contractility to KCl was increased by 33% in aortae of L2LPL mice. Maximal contraction to phenylephrine (PE) was comparable in L2 and L2LPL animals, while the frequency of tonus oscillation to PE increased by 104% in L2LPL mice.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In L2LPL animals, \u2022NO mediated relaxation to acetylcholine (ACh) and ATP was reduced by 47 and 32%, respectively. In contrast, endothelium\u2010independent relaxation to sodium nitroprusside (SNP) was not different in both groups tested.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>ATP\u2010initiated Ca<jats:sup>2+<\/jats:sup> elevation that triggers \u2022NO formation was increased by 41% in single aortic endothelial cells freshly isolated from L2LPL animals.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In aortae from L2LPL mice an increased \u2022O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> release occurred that was normalized by removing the endothelium and by the NAD(P)H oxidase inhibitor DPI and the PKC inhibitor GF109203X.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The reduced ACh\u2010induced relaxation in L2LPL animals was normalized in the presence of SOD, indicating that the reduced relaxation is due, at least in part, to enhanced \u2022NO scavenging by \u2022O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>These data suggest that despite normal lipoprotein levels increased LPL\u2010mediated FFAs loading initiates vascular dysfunction <jats:italic>via<\/jats:italic> PKC\u2010mediated activation of endothelial NAD(P)H oxidase. Thus, vascular LPL activity might represent a primary risk factor for atherosclerosis independently from cholesterol\/LDL levels.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2002) <jats:bold>135<\/jats:bold>, 143\u2013154; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0704440\">10.1038\/sj.bjp.0704440<\/jats:ext-link><\/jats:p>","DOI":"10.1038\/sj.bjp.0704440","type":"journal-article","created":{"date-parts":[[2006,6,7]],"date-time":"2006-06-07T19:20:37Z","timestamp":1149708037000},"page":"143-154","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Tissue\u2010specific expression of human lipoprotein lipase in the vascular system affects vascular reactivity in transgenic mice"],"prefix":"10.1111","volume":"135","author":[{"given":"Victor E","family":"Esenabhalu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mirza","family":"Cerimagic","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roland","family":"Malli","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karin","family":"Osibow","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanja","family":"Levak\u2010Frank","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maud","family":"Frieden","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wolfgang","family":"Sattler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerhard M","family":"Kostner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rudolf","family":"Zechner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wolfgang F","family":"Graier","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2009,1,29]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.100.14.1494"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI6117"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1007\/PL00000206"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/0021-9150(95)05582-H"},{"issue":"2","key":"e_1_2_7_6_1","first-page":"7","article-title":"Cellular mechanisms controlling EDRF\/NO formation in endothelial cells","volume":"86","author":"BUSSE R.","year":"1991","journal-title":"Basic Res. 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