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After 35 weeks, L-4F-treated mice, in the absence\/presence of pravastatin, had significantly smaller lymph nodes and glomerular tufts (<jats:italic>P<\/jats:italic><jats:sub><jats:italic>L<\/jats:italic>,<jats:italic>LP<\/jats:italic><\/jats:sub>&lt; 0.05), lower serum levels of IgG antibodies to double stranded DNA (dsDNA) (<jats:italic>P<\/jats:italic><jats:sub><jats:italic>L<\/jats:italic><\/jats:sub>&lt; 0.05) and oxidized phospholipids (oxPLs) (<jats:italic>P<\/jats:italic><jats:sub><jats:italic>L<\/jats:italic>,<jats:italic>LP<\/jats:italic><\/jats:sub>&lt; 0.005), and elevated total and vertebral bone mineral density (<jats:italic>P<\/jats:italic><jats:sub><jats:italic>L<\/jats:italic>,<jats:italic>LP<\/jats:italic><\/jats:sub>&lt; 0.01) compared to vehicle controls. Although all treatment groups presented larger aortic root lesions compared to vehicle controls, enlarged atheromas in combination treatment mice had significantly less infiltrated CD68<jats:sup>+<\/jats:sup>macrophages (<jats:italic>P<\/jats:italic><jats:sub><jats:italic>LP<\/jats:italic><\/jats:sub>&lt; 0.01), significantly increased mean \u03b1-actin stained area (<jats:italic>P<\/jats:italic><jats:sub><jats:italic>LP<\/jats:italic><\/jats:sub>&lt; 0.05), and significantly lower levels of circulating markers for atherosclerosis progression, CCL19 (<jats:italic>P<\/jats:italic><jats:sub><jats:italic>L<\/jats:italic>,<jats:italic>LP<\/jats:italic><\/jats:sub>&lt; 0.0005) and VCAM-1 (<jats:italic>P<\/jats:italic><jats:sub><jats:italic>L<\/jats:italic><\/jats:sub>&lt; 0.0002).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>L-4F treatment, alone or with pravastatin, significantly reduced IgG anti-dsDNA and IgG anti-oxPLs, proteinuria, glomerulonephritis, and osteopenia in a murine lupus model of accelerated atherosclerosis. Despite enlarged aortic lesions, increased smooth muscle content, decreased macrophage infiltration, and decreased pro-atherogenic chemokines in L-4F plus pravastatin treated mice suggest protective mechanisms not only on lupus-like disease, but also on potential plaque remodeling in a murine model of systemic lupus erythematosus (SLE) and accelerated atherosclerosis.<\/jats:p><\/jats:sec>","DOI":"10.1186\/ar3020","type":"journal-article","created":{"date-parts":[[2010,5,18]],"date-time":"2010-05-18T18:15:10Z","timestamp":1274206510000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":46,"title":["Treatment with apolipoprotein A-1 mimetic peptide reduces lupus-like manifestations in a murine lupus model of accelerated atherosclerosis"],"prefix":"10.1186","volume":"12","author":[{"given":"Jennifer MP","family":"Woo","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhuofeng","family":"Lin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mohamad","family":"Navab","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Casey","family":"Van Dyck","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yvette","family":"Trejo-Lopez","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Krystal MT","family":"Woo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hongyun","family":"Li","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lawrence W","family":"Castellani","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xuping","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Noriko","family":"Iikuni","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ornella J","family":"Rullo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hui","family":"Wu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Antonio","family":"La Cava","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alan M","family":"Fogelman","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Aldons J","family":"Lusis","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Betty P","family":"Tsao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2010,5,18]]},"reference":[{"key":"2855_CR1","doi-asserted-by":"publisher","first-page":"2331","DOI":"10.1002\/1529-0131(200110)44:10<2331::AID-ART395>3.0.CO;2-I","volume":"44","author":"JM Esdaile","year":"2001","unstructured":"Esdaile JM, Abrahamowicz M, Grodzicky T, Li Y, Panaritis C, du Berger R, C\u00f4te R, Grover SA, Fortin PR, Clarke AE, Sen\u00e9cal JL: Traditional Framingham risk factors fail to fully account for accelerated atherosclerosis in systemic lupus erythematosus. 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