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The anti-TNF-α antibody infliximab inhibits the expression of fat-transporter-protein FAT/CD36 in a selective hepatic-radiation mouse model.

dc.contributor.authorMartius, Gesa
dc.contributor.authorCameron, Silke
dc.contributor.authorRave-Fränk, Margret
dc.contributor.authorHess, Clemens F.
dc.contributor.authorWolff, Hendrik A.
dc.contributor.authorMalik, Ihtzaz A.
dc.date.accessioned2015-05-08T08:36:47Z
dc.date.available2015-05-08T08:36:47Z
dc.date.issued2015
dc.identifier.citationMartius, Gesa; Cameron, Silke; Rave-Fränk, Margret; Hess, Clemens F; Wolff, Hendrik A; Malik, Ihtzaz A (2015): The anti-TNF-α antibody infliximab inhibits the expression of fat-transporter-protein FAT/CD36 in a selective hepatic-radiation mouse model. - International journal of molecular sciences, Vol. 16, Nr. 3, p. 4682-97
dc.relation.ISSN1422-0067
dc.identifier.urihttp://resolver.sub.uni-goettingen.de/purl?gs-1/11783
dc.description.abstractPreviously, we reported a radiation-induced inflammation triggering fat-accumulation through fatty-acid-translocase/cluster of differentiation protein 36 (FAT/CD36) in rat liver. Furthermore, inhibition of radiation-induced FAT/CD36-expression by anti-tumor necrosis factor-α (anti-TNF-α) (infliximab) was shown in vitro. The current study investigates fat-accumulation in a mouse-model of single-dose liver-irradiation (25-Gray) and the effect of anti-TNF-α-therapy on FAT/CD36 gene-expression. Mice livers were selectively irradiated in vivo in presence or absence of infliximab. Serum- and hepatic-triglycerides, mRNA, and protein were analyzed by colorimetric assays, RT-PCR, Immunofluorescence and Western-Blot, respectively. Sudan-staining was used demonstrating fat-accumulation in tissue. In mice livers, early (1-3 h) induction of TNF-α-expression, a pro-inflammatory cytokine, was observed. It was followed by elevated hepatic-triglyceride level (6-12 h), compared to sham-irradiated controls. In contrast, serum-triglyceride level was decreased at these time points. Similar to triglyceride level in mice livers, Sudan staining of liver cryosections showed a quick (6-12 h) increase of fat-droplets after irradiation. Furthermore, expression of fat-transporter-protein FAT/CD36 was increased at protein level caused by radiation or TNF-α. TNF-α-blockage by anti-TNF-α showed an early inhibition of radiation-induced FAT/CD36 expression in mice livers. Immunohistochemistry showed basolateral and cytoplasmic expression of FAT/CD36 in hepatocytes. Moreover, co-localization of FAT/CD36 was detected with α-smooth muscle actin (α-SMA+) cells and F4/80+ macrophages. In summary, hepatic-radiation triggers fat-accumulation in mice livers, involving acute-phase-processes. Accordingly, anti-TNF-α-therapy prevented early radiation-induced expression of FAT/CD36 in vivo.
dc.description.sponsorshipOpen-Access-Publikationsfonds 2015
dc.languageeng
dc.language.isoeng
dc.rightsopenAccess
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectirradiation; fat accumulation; liver; FAT/CD36; TNF-α; infliximab
dc.titleThe anti-TNF-α antibody infliximab inhibits the expression of fat-transporter-protein FAT/CD36 in a selective hepatic-radiation mouse model.
dc.typejournalArticle
dc.identifier.doi10.3390/ijms16034682
dc.type.versionpublishedVersion
dc.bibliographicCitation.volume16
dc.bibliographicCitation.issue3
dc.bibliographicCitation.firstPage4682
dc.bibliographicCitation.lastPage4697
dc.type.subtypejournalArticle
dc.identifier.pmid25739082
dc.description.statuspeerReviewed
dc.bibliographicCitation.journalInternational journal of molecular sciences


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