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All-trans retinoic acid regulates CXCL16/SR-PSOX expression
University of Örebro, Sweden.
University of Örebro, Sweden.
University of Örebro, Sweden.
2005 (Engelska)Ingår i: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 16, nr 4, s. 661-665Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Several studies have shown the ability of retinoids to modulate inflammatory response. CXCL16/SR-PSOX is a novel protein functioning as a chemokine and a scavenger receptor. We investigated effects of all-trans retinoic acid (atRA) on CXCL16/SR-PSOX expression in several cell types. Real-time PCR showed that atRA increased CXCL16/SRPSOX mRNA expression in THP-1 and endothelial cells, which corresponded to increased release of CXCL16 protein from the cells, measured by ELISA. In THP-1 cells this effect was reduced by retinoic acid receptor (RAR) antagonist, which indicates receptor-mediated inhibition. RAR-alpha and RAR-gamma agonists increased CXCL16 release, which suggests RAR-mediated effect of atRA, which is not selective for a particular RAR subtype. In smooth muscle cells, up-regulation of CXCL16 mRNA was observed only after 96 h of treatment, while protein expression did not change. These findings suggest that retinoid signaling might be a pathway modulating inflammatory response by regulating CXCL16 expression in a cell-specific manner.

Ort, förlag, år, upplaga, sidor
Spandidos Publications , 2005. Vol. 16, nr 4, s. 661-665
Nyckelord [en]
chemokines; inflammation; CXCL16/SR-PSOX; retinoids; all-trans retinoic acid; retinoic acid receptor; THP-1 cells; HUVEC; AOSMC
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
URN: urn:nbn:se:liu:diva-100357ISI: 000232087900023PubMedID: 16142401OAI: oai:DiVA.org:liu-100357DiVA, id: diva2:661606
Tillgänglig från: 2013-11-04 Skapad: 2013-11-04 Senast uppdaterad: 2017-12-06Bibliografiskt granskad

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