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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:739.)
© 2008 American Heart Association, Inc.

Cell Biology/Signaling

Far Infrared Therapy Inhibits Vascular Endothelial Inflammation via the Induction of Heme Oxygenase-1

Chih-Ching Lin; Xiao-Ming Liu; Kelly Peyton; Hong Wang; Wu-Chang Yang; Shing-Jong Lin; William Durante

From the Institute of Clinical Medicine (C.-C.L., S.-J.L.), School of Medicine (C.-C.L., W.-C.Y., S.-J.L.), National Yang-Ming University, Taipei, Taiwan; the Division of Nephrology (C.-C.L., W.-C.Y.) and the Division of Cardiology (S.-J.L.), Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan; the Division of Nephrology, Department of Medicine, National Yang-Ming University Hospital, I-Ian, Taiwan; the Department of Pharmacology (H.W.), Temple University, Philadelphia, Pa; and the Department of Medical Pharmacology and Physiology (X.M.L., K.P., W.D.), School of Medicine, University of Missouri-Columbia, Columbia, Mo.

Correspondence to William Durante, PhD, Department of Medical Pharmacology and Physiology, M409 Medical Science Building, University of Missouri-Columbia, One Hospital Drive, Columbia, MO 65212. E-mail durantew{at}health.missouri.edu

Objective— Survival of arteriovenous fistulas (AVFs) in hemodialysis patients is associated with both far infrared (FIR) therapy and length polymorphisms of the heme oxygenase-1 (HO-1) promoter. In this study, we evaluated whether there is an interaction between FIR radiation and HO-1 in regulating vascular inflammation.

Methods and Results— Treatment of cultured human umbilical vein endothelial cells (ECs) with FIR radiation stimulated HO-1 protein, mRNA, and promoter activity. HO-1 induction was dependent on the activation of the antioxidant responsive element/NF-E2-related factor-2 complex, and was likely a consequence of heat stress. FIR radiation also inhibited tumor necrosis factor (TNF)-–mediated expression of E-selectin, vascular cell adhesion molecule-1, intercellular cell adhesion molecule-1, monocyte chemoattractant protein-1, interleukin-8, and the cytokine-mediated adhesion of monocytes to ECs. The antiinflammatory action of FIR was mimicked by bilirubin, and was reversed by the HO inhibitor, tin protoporphyrin-IX, or by the selective knockdown of HO-1. Finally, the antiinflammatory effect of FIR was also observed in patients undergoing hemodialysis.

Conclusions— These results demonstrate that FIR therapy exerts a potent antiinflammatory effect via the induction of HO-1. The ability of FIR therapy to inhibit inflammation may play a critical role in preserving blood flow and patency of AVFs in hemodialysis patients.

Far infrared (FIR) therapy improves survival of arteriovenous fistulas in hemodialysis patients, but the underlying mechanism is unknown. We now report that FIR radiation stimulates heme oxygenase-1 (HO-1) expression in endothelial cell and that the induction of HO-1 confers antiinflammatory actions that may underlie the beneficial effects of FIR therapy.

Key Words: endothelium • far infrared therapy • inflammation • leukocyte adhesion

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