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Osteopontin (OPN) has been implicated in the pathology of several renal conditions. This study was to evaluate the effects of OPN on hypercholesterolemia induced renal dysfunction. Eight-week-old male mice were divided into 4 groups: apolipoprotein E knockout (ApoE<jats:sup>\u2212\/\u2212<\/jats:sup>) and ApoE\/OPN knockout (ApoE<jats:sup>\u2212\/\u2212<\/jats:sup>\/OPN<jats:sup>\u2212\/\u2212<\/jats:sup>) mice fed a normal diet (ND) or high cholesterol diet (HD). After 4 weeks, Periodic acid-Schiff (PAS) and oil red O staining revealed excessive lipid deposition in the glomeruli of ApoE<jats:sup>\u2212\/\u2212<\/jats:sup>HD mice, however, significantly suppressed in ApoE<jats:sup>\u2212\/\u2212<\/jats:sup>\/OPN<jats:sup>\u2212\/\u2212<\/jats:sup>HD mice. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) expression was lower in the glomeruli of ApoE<jats:sup>\u2212\/\u2212<\/jats:sup>\/OPN<jats:sup>\u2212\/\u2212<\/jats:sup>HD mice than ApoE<jats:sup>\u2212\/\u2212<\/jats:sup>HD mice. <jats:italic>In vitro<\/jats:italic> study, primary mesangial cells were incubated with recombinant mouse OPN (rmOPN). RmOPN induced LOX-1 mRNA and protein expression in primary mesangial cells. Pre-treatment with an ERK inhibitor suppressed the LOX-1 gene expression induced by rmOPN. These results indicate that OPN contributes to kidney damage in hypercholesterolemia and suggest that inhibition of OPN may provide a potential therapeutic target for the prevention of hypercholesterolemia.<\/jats:p>","DOI":"10.1038\/srep28882","type":"journal-article","created":{"date-parts":[[2016,6,29]],"date-time":"2016-06-29T10:06:57Z","timestamp":1467194817000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Osteopontin deficiency reduces kidney damage from hypercholesterolemia in Apolipoprotein E-deficient mice"],"prefix":"10.1038","volume":"6","author":[{"given":"Zouwei","family":"Pei","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takafumi","family":"Okura","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomoaki","family":"Nagao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daijiro","family":"Enomoto","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masayoshi","family":"Kukida","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Akiko","family":"Tanino","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ken-ichi","family":"Miyoshi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mie","family":"Kurata","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jitsuo","family":"Higaki","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2016,6,29]]},"reference":[{"key":"BFsrep28882_CR1","doi-asserted-by":"crossref","first-page":"4471","DOI":"10.1073\/pnas.89.10.4471","volume":"89","author":"JA Piedrahita","year":"1992","unstructured":"Piedrahita, J. 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Co. and DaiNihon-Sumitomo Co. The other authors have indicated that they have no conflicts of interest with regards to the contents of this article.","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"28882"}}