All-trans retinoic acid regulates CXCL16/SR-PSOX expression

  • Authors:
    • Dick Wågsäter
    • Yuri Shelikine
    • Allan Sirsjö
  • View Affiliations

  • Published online on: October 1, 2005     https://doi.org/10.3892/ijmm.16.4.661
  • Pages: 661-665
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Abstract

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/SR-PSOX 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-α and RAR-γ 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.

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October 2005
Volume 16 Issue 4

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Wågsäter D, Shelikine Y and Sirsjö A: All-trans retinoic acid regulates CXCL16/SR-PSOX expression. Int J Mol Med 16: 661-665, 2005.
APA
Wågsäter, D., Shelikine, Y., & Sirsjö, A. (2005). All-trans retinoic acid regulates CXCL16/SR-PSOX expression. International Journal of Molecular Medicine, 16, 661-665. https://doi.org/10.3892/ijmm.16.4.661
MLA
Wågsäter, D., Shelikine, Y., Sirsjö, A."All-trans retinoic acid regulates CXCL16/SR-PSOX expression". International Journal of Molecular Medicine 16.4 (2005): 661-665.
Chicago
Wågsäter, D., Shelikine, Y., Sirsjö, A."All-trans retinoic acid regulates CXCL16/SR-PSOX expression". International Journal of Molecular Medicine 16, no. 4 (2005): 661-665. https://doi.org/10.3892/ijmm.16.4.661