The role of osteopontin in d-galactosamine-induced liver injury in genetically obese mice

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dc.contributor.authorHyo Jung Kwon-
dc.contributor.authorYoung Suk Won-
dc.contributor.authorWoon Kee Yoon-
dc.contributor.authorKi Hoan Nam-
dc.contributor.authorD Y Kim-
dc.contributor.authorHyoung-Chin Kim-
dc.date.accessioned2017-04-19T09:17:12Z-
dc.date.available2017-04-19T09:17:12Z-
dc.date.issued2010-
dc.identifier.issn0041-008X-
dc.identifier.uri10.1016/j.taap.2009.11.006ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/9340-
dc.description.abstractVarious epidemiological studies have shown that obesity increases the risk of liver disease, but the precise mechanisms through which this occurs are poorly understood. In the present study, we hypothesized that osteopontin (OPN), an extracellular matrix and proinflammatory cytokine, has an important role in making obese mice more susceptible to inflammatory liver injury. After exposure of genetically obese ob/ob and db/db mice to a single dose of d-galactosamine (GalN), the plasma liver enzyme levels, histology and expression levels of cytokines and OPN were evaluated. The ob/ob and db/db mice, which were more sensitive to GalN-induced inflammatory liver injury compared with wild-type mice, had significantly higher plasma and hepatic OPN expression levels. Increased OPN expression was mainly found in hepatocytes and inflammatory cells and was correlated with markedly up-regulated interleukin (IL)-12 and IL-18 levels. Furthermore, pretreatment with a neutralizing OPN (nOPN) antibody attenuated the GalN-induced inflammatory liver injury in ob/ob and db/db mice, which was accompanied by significantly reduced macrophages recruitment and IL-12 and IL-18 productions. Taken together, these results suggest that up-regulated OPN expression is a contributing factor to increased susceptibility of genetically obese mice to GalN-induced liver injury by promoting inflammation and modulating immune response.-
dc.publisherElsevier-
dc.titleThe role of osteopontin in d-galactosamine-induced liver injury in genetically obese mice-
dc.title.alternativeThe role of osteopontin in d-galactosamine-induced liver injury in genetically obese mice-
dc.typeArticle-
dc.citation.titleToxicology and Applied Pharmacology-
dc.citation.number3-
dc.citation.endPage351-
dc.citation.startPage344-
dc.citation.volume242-
dc.contributor.affiliatedAuthorHyo Jung Kwon-
dc.contributor.affiliatedAuthorYoung Suk Won-
dc.contributor.affiliatedAuthorWoon Kee Yoon-
dc.contributor.affiliatedAuthorKi Hoan Nam-
dc.contributor.affiliatedAuthorHyoung-Chin Kim-
dc.contributor.alternativeName권효정-
dc.contributor.alternativeName원영석-
dc.contributor.alternativeName윤원기-
dc.contributor.alternativeName남기환-
dc.contributor.alternativeName김대용-
dc.contributor.alternativeName김형진-
dc.identifier.bibliographicCitationToxicology and Applied Pharmacology, vol. 242, no. 3, pp. 344-351-
dc.identifier.doi10.1016/j.taap.2009.11.006-
dc.subject.keywordd-Galactosamine-
dc.subject.keywordInterleukin-12-
dc.subject.keywordInterleukin-18-
dc.subject.keywordObese mice-
dc.subject.keywordOsteopontin-
dc.subject.localD-galactosamine-
dc.subject.locald-Galactosamine-
dc.subject.localInterleukin-12-
dc.subject.localinterleukin-12-
dc.subject.localinterleukin-18-
dc.subject.localInterleukin-18-
dc.subject.localObese mice-
dc.subject.localOsteopontin-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
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