首页|Calcium influx through TRPV4 channels involve in hyperosmotic stress-induced epithelial-mesenchymal transition in tubular epithelial cells
Calcium influx through TRPV4 channels involve in hyperosmotic stress-induced epithelial-mesenchymal transition in tubular epithelial cells
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NSTL
The epithelial-mesenchymal transition (EMT) is a biological process that occurs in the pathogenesis of kidney diseases in which injured tubular epithelial cells transform into myofibroblasts。 We previously showed that mannitol-mediated hyperosmotic stress induces EMT of tubular epithelial cells。 Although Ca2+ signaling is essential for the induction of EMT in tubular epithelial cells， the role of specific calcium channels is unknown。 In this study， we assessed the transient receptor potential vanilloid 4 (TRPV4)-mediated Ca2+ influx in the hyperosmolarity-induced EMT。 The Fluo-4 assay was used to examine the effect of hyperosmotic stress on the intracellular Ca2+ level of normal rat kidney (NRK)-52E cells。 Expression of a mesenchymal marker a-smooth muscle actin (a-SMA) and an epithelial marker E-cadherin was also observed by fluorescence microscopy。 The hyperosmotic stress caused a transient increase in intracellular Ca2+ concentration as well as a decrease in E-cadherin and an increase in a-SMA expressions in tubular epithelial cells， indicating the induction of EMT。 A TRPV4 channel antagonist inhibited hyperosmotic stress-induced Ca2+ influx and the EMT， whereas， a TRPV4 channel agonist increased Ca2+ influx and EMT induction in tubular epithelial cells without the hyperosmotic stress。 These findings suggest that Ca2+ influx through TRPV4 channels contributes to the hyperosmotic stress-induced EMT of tubular epithelial cells。
NSTL
