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LDL(\u2212), isolated by anion-exchange chromatography, differed from nonelectronegative LDL [LDL(+)] in its higher triglyceride, nonesterified fatty acid, apoprotein E and apoprotein C-III, and sialic acid contents. No evidence of extensive oxidation was found in LDL(\u2212); its antioxidant and thiobarbituric acid\u2013reactive substances contents were similar to those of LDL(+). However, conjugated dienes were increased in LDL(\u2212), which suggests that mild oxidation might affect these particles. LDL(\u2212) increased, in a concentration-dependent manner, the release of IL-8 and MCP-1 by ECs and was a stronger inductor of both chemokines than oxidized LDL (oxLDL) or LDL(+). PAI-1 release increased slightly in ECs incubated with both LDL(\u2212) and oxLDL but not with LDL(+). However, no cytotoxic effects of LDL(\u2212) were observed on ECs. Actinomycin D inhibited the release of IL-8 and MCP-1 induced by LDL(\u2212) and oxLDL by up to 80%, indicating that their production is mediated by protein synthesis. Incubation of ECs with<jats:italic>N<\/jats:italic>-acetyl cysteine inhibited production of IL-8 and MCP-1 induced by LDL(\u2212) and oxLDL by &gt;50%. The free radical scavenger butylated hydroxytoluene slightly inhibited the effect of oxLDL but did not modify the effect of LDL(\u2212). An antagonist (BN-50730) of the platelet-activating factor receptor inhibited production of both chemokines by LDL(\u2212) and oxLDL in a concentration-dependent manner. Our results indicate that LDL(\u2212) shows proinflammatory activity on ECs and may contribute to early atherosclerotic events.<\/jats:p>","DOI":"10.1161\/01.atv.20.10.2281","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T19:44:19Z","timestamp":1308339859000},"page":"2281-2287","source":"Crossref","is-referenced-by-count":93,"title":["Electronegative LDL From Normolipemic Subjects Induces IL-8 and Monocyte Chemotactic Protein Secretion by Human Endothelial Cells"],"prefix":"10.1161","volume":"20","author":[{"family":"Conxita De Castellarnau","sequence":"first","affiliation":[{"name":"From the Institut de Recerca (C.d.C., R.R., L.C., L.V.) and Servei de Bioqui\u0301mica (J.L.S-Q, S.B., J.O-Ll.), Hospital de la Santa Creu i Sant Pau, Departament de Bioqui\u0301mica i Biologi\u0301a Molecular (S.B., J.O.-Ll.), Universitat Auto\u0300noma, Barcelona, Spain."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jose\u0301 Luis","family":"Sa\u0301nchez-Quesada","sequence":"additional","affiliation":[{"name":"From the Institut de Recerca (C.d.C., R.R., L.C., L.V.) and Servei de Bioqui\u0301mica (J.L.S-Q, S.B., J.O-Ll.), Hospital de la Santa Creu i Sant Pau, Departament de Bioqui\u0301mica i Biologi\u0301a Molecular (S.B., J.O.-Ll.), Universitat Auto\u0300noma, Barcelona, Spain."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sonia","family":"Beni\u0301tez","sequence":"additional","affiliation":[{"name":"From the Institut de Recerca (C.d.C., R.R., L.C., L.V.) and Servei de Bioqui\u0301mica (J.L.S-Q, S.B., J.O-Ll.), Hospital de la Santa Creu i Sant Pau, Departament de Bioqui\u0301mica i Biologi\u0301a Molecular (S.B., J.O.-Ll.), Universitat Auto\u0300noma, Barcelona, Spain."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roser","family":"Rosa","sequence":"additional","affiliation":[{"name":"From the Institut de Recerca (C.d.C., R.R., L.C., L.V.) and Servei de 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