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Acta Physiologica 2007; Volume 189, Supplement 653
The 86th Annual Meeting of The German Physiological Society
3/25/2007-3/28/2007
Hannover, Germany
CAPSAICIN INDUCES CA2+ INFLUX IN HUMAN CORNEAL EPITHELIAL CELLS BY ACTIVATING TRPV1 CHANNELS
Abstract number: P16-L5-11
Mergler1 S, Zhang F, Yang H, Pan Z, Pleyer1 U, Reinach P
1Charit Universittsmedizin Berlin, Dept. of Ophthalmology
State University of New York, College of Optometry, 33 West 42nd Street, New York, NY 10036, U.S.A
TRPV1, a member of the vanilloid-type transient receptor potential ion channel family, is activated by heat or by the agonist capsaicin. Exposure of TRPV1 to capsaicin results in an increase in intracellular free Ca2+ ([Ca2+]i). Capsaicin is a most potent activator of TRPV1. We recently detected TRPs in human corneal epithelial cells (HCEC-SV40). However, the role of TRPs in these cells remains unknown. In this study, we investigated effects of capsaicin on [Ca2+]i and non-selective cation channel currents. The protein expression of TRPV1 was identified by Western blotting. The effects of capsaicin were determined by cell fluorescence imaging and whole-cell patch-clamp technique. Capsaicin (10 mM) increased [Ca2+]i. The fluorescence ratio
(f340/f380) was 1.2086 ± 0.0044 in the resting state (n = 3). After application of capsaicin for 10 min it increased to 1.2721 ±?0.0039 (n = 4; p < 0.01). In addition, cation channel currents increased to 252 ± 51 % of control (set to 100 %) (n = 6; p <?0.05). In conclusion, capsaicin induces significant increases of non-selective cation channel currents through TRPV1 in HCEC- SV40. Potentially, TRPV1 may play a role in pathophysiology of these cells.
To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 189, Supplement 653 :P16-L5-11