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KMID : 0613820110210050664
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Journal of Life Science
2011 Volume.21 No. 5 p.664 ~ p.670
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Vascular Smooth Muscle Cells Secrete CXCL10 in Response to Heat Shock Protein 90
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Rhim Byung-Yong
Kim Do-Hyung
Kim Koan-Hoi
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Abstract
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Oxidative stress results in sustained release of heat shock protein 90 (HSP90) from vascular smooth muscle cells (VSMCs). We investigated whether extracellular HSP90 predisposed VSMCs to pro-inflammatory phenotype. Exposure of human aortic smooth muscle cells to HSP90 not only significantly enhanced CXCL10 secretion but also increased CXCL10 transcription. HSP90-mediated CXCL10 secretion was attenuated by OxPAPC, a TLR-2/4 inhibitor, and curcumin, a TLR-4 dimerization inhibitor. Inhibitors of diphenyleneiodium chloride and the Akt pathway also attenuated CXCL10 secretion in response to HSP90. The gene delivery of IκB using recombinant adenoviruses and treatment with resveratrol, which inhibit NF-κB activity, significantly attenuated HSP90-induced CXCL10 secretion from VSMCs. We propose that extracellular HSP90 contributes to an inflammatory reaction in the stressed vasculature by inducing CXCL10 expression of VSMCs, and that TLR-4, Akt, and NF-κB play active roles in the process.
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KEYWORD
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CXCL10, HSP90, vascular smooth muscle cells
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