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Role of Reactive Oxygen Species and Redox in Regulating the Function of Transient Receptor Potential Channels

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posted on 07.05.2011 by Michael Y. Song, Ayako Mainko, Jason X.-J. Yuan
Cellular redox status, regulated by production of reactive oxygen species (ROS), greatly contributes to the regulation of vascular smooth muscle cell contraction, migration, proliferation, and apoptosis by modulating the function of transient receptor potential (TRP) channels in the plasma membrane. ROS functionally interact with the channel protein via oxidizing the redox-sensitive residues, whereas nitric oxide (NO) regulates TRP channel function by cyclic GMP/protein kinase G-dependent and -independent pathways. Based on the structural differences among different TRP isoforms, the effects of ROS and NO are also different. In addition to regulating TRP channels in the plasma membrane, ROS and NO also modulate Ca2+ release channels (e.g., IP3 and ryanodine receptors) on the sarcoplasmic/endoplasmic reticulum membrane. This review aims at briefly describing (a) the role of TRP channels in receptor-operated and store-operated Ca2+ entry, and (b) the role of ROS and redox status in regulating the function and structure of TRP channels.

Funding

This work was supported in part by grants from the National Institutes of Health (HL054043 and HL066012 to J.X.-J.Y., and DK083506 to A.M.). M.Y.S. is supported by an NIH training grant (T32 DK007202).

History

Publisher Statement

This is a copy of an article published in the Antioxidants and Redox Signaling © 2011 Copyright Mary Ann Liebert, Inc.]; Antioxidants and Redox Signaling is available online at: http://www.liebertonline.com. The final version is available through Mary Ann Liebert at DOI: 10.1089/ars.2010.3648

Publisher

Mary Ann Liebert

Language

en_US

issn

1557-7716

Issue date

11/04/2011

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