Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/112842
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dc.contributor.authorVangaveti, V.en
dc.contributor.authorShashidhar, V.en
dc.contributor.authorCollier, F.en
dc.contributor.authorHodge, J.en
dc.contributor.authorRush, C.en
dc.contributor.authorMalabu, U.en
dc.contributor.authorBaune, B.en
dc.contributor.authorKennedy, R.en
dc.date.issued2018en
dc.identifier.citationTherapeutic Advances in Endocrinology and Metabolism, 2018; 9(5):137-150en
dc.identifier.issn2042-0188en
dc.identifier.issn2042-0196en
dc.identifier.urihttp://hdl.handle.net/2440/112842-
dc.description.abstractBackground: Both activation of monocytes and increased serum fatty acid binding protein-4 (FABP4) occur in diabetes and are associated with increased atherosclerosis. The oxidized lipid, 9-hydroxyoctadecadienoic acid (9-HODE) increases FABP4 in macrophages, and is a ligand for G protein-coupled receptor 132 (GPR132). We investigated the involvement of GPR132 in mediating the 9-, 13-HODE stimulation of FABP4 secretion, and whether GPR132 expression is increased in monocytes from patients with type 2 diabetes. Methods: The effects of siRNA silencing of GPR132 gene and of the PPAR-γ antagonist T0070907 were studied in THP-1 cells. Serum levels of FABP4 and other adipokines were measured in patients with diabetes, and monocyte subpopulations were analyzed using flow cytometry. GPR132 mRNA was quantified in isolated CD14+ cells. Results: 9-HODE and 13-HODE increased FABP4 expression in THP-1 monocytes and macrophages, and also increased GPR132 expression. Silencing of GPR132 did not influence the increase in FABP4 with 9-HODE, 13-HODE, or rosiglitazone (ROSI). By contrast, T0070907 inhibited the effect of all three ligands on FABP4 expression. Diabetic subjects had increased serum FABP4, and activated monocytes. They also expressed higher levels of GPR132 mRNA in CD14+ cells. Conclusions: We conclude that GPR132 is an independent monocyte activation marker in diabetes, but does not contribute to PPAR-γ-mediated induction of FABP4 by HODEs.en
dc.description.statementofresponsibilityVenkat Vangaveti , Venkatesh Shashidhar, Fiona Collier, Jason Hodge, Catherine Rush, Usman Malabu, Bernhard Baune and Richard Lee Kennedyen
dc.language.isoenen
dc.publisherSAGE Publishingen
dc.rights© The Author(s), 2018.en
dc.subjectFABP4; HODEs; macrophagesen
dc.title9- and 13-HODE regulate fatty acid binding protein-4 in human macrophages, but does not involve HODE/GPR132 axis in PPAR-γ regulation of FABP4en
dc.title.alternative9- and 13-HODE regulate fatty acid binding protein-4 in human macrophages, but does not involve HODE/GPR132 axis in PPAR-gamma regulation of FABP4en
dc.typeJournal articleen
dc.identifier.rmid0030090029en
dc.identifier.doi10.1177/2042018818759894en
dc.identifier.pubid422018-
pubs.library.collectionMedicine publicationsen
pubs.library.teamDS10en
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidBaune, B. [0000-0001-6548-426X]en
Appears in Collections:Medicine publications

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