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J Biol Chem. 2010 Jun 11;285(24):18749-58. doi: 10.1074/jbc.M110.103606. Epub 2010 Apr 22.

The TRPV4 channel contributes to intercellular junction formation in keratinocytes.

Author information

1
Division of Cell Signaling, Okazaki Institute for Integrative Bioscience, National Institute for Physiological Sciences, National Institutes of Natural Sciences, Okazaki 444-8787, Japan. sokabe@nips.ac.jp

Abstract

Transient receptor potential vanilloid 4 (TRPV4) channel is a physiological sensor for hypo-osmolarity, mechanical deformation, and warm temperature. The channel activation leads to various cellular effects involving Ca(2+) dynamics. We found that TRPV4 interacts with beta-catenin, a crucial component linking adherens junctions and the actin cytoskeleton, thereby enhancing cell-cell junction development and formation of the tight barrier between skin keratinocytes. TRPV4-deficient mice displayed impairment of the intercellular junction-dependent barrier function in the skin. In TRPV4-deficient keratinocytes, extracellular Ca(2+)-induced actin rearrangement and stratification were delayed following significant reduction in cytosolic Ca(2+) increase and small GTPase Rho activation. TRPV4 protein located where the cell-cell junctions are formed, and the channel deficiency caused abnormal cell-cell junction structures, resulting in higher intercellular permeability in vitro. Our results suggest a novel role for TRPV4 in the development and maturation of cell-cell junctions in epithelia of the skin.

PMID:
20413591
PMCID:
PMC2881798
DOI:
10.1074/jbc.M110.103606
[Indexed for MEDLINE]
Free PMC Article

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