Regulation of the human short transient receptor potential channel 3 (htrp3)‎ by the serum-and glucocorticoid-induced kinase 1 (SGK1)‎

Abstract EN

The transient receptor potential channels (TRP channels) are widely expressed in a large number of various human and animal cell types.

Most of the TRP channels are permeable for Ca2+ and some also for Mg2+.

TRP channels are divided into three main groups based on their structure: short, long and osm-like TRPs.

The short TRP subfamily of cation channels contains mammalian TRPs, TRPL, and the Drosophila TRP.

The mammalian TRP superfamily of cation channels contains four subfamilies (TRP1; TRP4, 5; TRP2 and TRP3, 6, 7) based on sufficiently similar sequence and function.

The human short transient receptor potential channel 3 (hTRP3) is expressed at the highest levels in brain, and at much lower levels in small intestine, colon, testis, prostate, ovary, placenta and lung.

Cytosolic Ca2+ ([Ca2+]i) plays a crucial role in various cellular functions of virtually all cell types and is thus under tight hormonal control.

However, cellular mechanisms governing the regulation of human TRP3 abundance in the cell membrane are poorly understood.

Surface abundance of the epithelial Na+ channel is regulated by the Serum- and Glucocorticoid-Induced Kinase 1 (SGK1).

The present study has been performed to explore whether human TRP3 is regulated by SGK1 and the related kinases SGK2, and SGK3.

To this end, cRNA encoding human TRP3 (hTRP3) has been injected with or without cRNA encoding wild type SGK1, SGK2, and SGK3 into Xenopus Oocytes.

In the presence of Cl-, hTRP3 mediated Ca2+ entry leads to secondary activation of Ca2+-sensitive Cl- channels (ICl(Ca)).

Coexpression of hTRP3 with SGK1 stimulates (ICl(Ca)) but not by SGK2, and SGK3.

The observations suggest that SGK1 regulate hTRP3 and are thus likely to participate in the regulation of calcium homeostasis.