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The anti‐inflammatory Cytokine IL‐19 induces HO‐1 Expression and Decreases Reactive Oxygen Species in human Vascular Smooth muscle cells
Author(s) -
Gabunia Khatuna,
Kelemen Sheri,
Ellison Stephen,
Autieri Michael
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.616.8
Heme oxygenase‐1 (HO‐1) has potent anti‐inflammatory activity and recognized vascular protective effects. We have recently described the expression and vascular protective effects of an anti‐inflammatory interleukin (IL‐19), in vascular smooth muscle cells (VSMC) and injured arteries. The objective of this study was to characterize the expression and protective effects of IL‐19‐induced HO‐1 in VSMC. HO‐1 mRNA was induced in IL‐19 stimulated cultured human VSMC, as assayed by quantitative RT‐PCR. HO‐1 protein was induced 700%, as assayed by western blot. HO‐1 concentrations rapidly increase from 9.0 pg/mg protein to 46 pg/mg protein in IL‐19 stimulated VSMC as assayed by ELISA. IL‐19 does not induce HO‐1 mRNA or protein in human Endothelial cells. IL‐19 activates STAT3 in VSMC, and IL‐19‐induced HO‐1 expression is significantly reduced by transfection of VSMC with STAT3 siRNA. HO‐1 attenuates reactive oxy, but ROS is not decreased by IL‐19 in VSMC in which HO‐1 is reduced by siRNA, indicating that the IL‐19 driven reduction in ROS is mediated by HO‐1 expression. IL‐19 treatment can reduce apoptosis induced by serum deprivation by 50%, as assayed by Annexin IV flow cytometry. These data indicate that IL‐19 can reduce ROS and apoptosis in hVSMC, which may be mediated by IL‐19 induction of HO‐1expression. This points to IL‐19 as a potential therapeutic for vascular inflammatory diseases.