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MironRNA‐194 (mir‐194) regulates ROMk channel activity by down‐regulation of intersectin 1 (ITSN1)‐WNK pathway
Author(s) -
Lin Daohong,
Yue Peng,
Wang Wenhui
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb754
Subject(s) - hek 293 cells , chemistry , microbiology and biotechnology , western blot , potassium channel , downregulation and upregulation , endocrinology , biology , gene , biochemistry
The aim of the present study is to test whether miR‐194 plays a role in mediating the effect of high K (HK) intake on ROMK channels through inhibiting ITSN1‐dependent endocytosis of ROMK channels. Northern blot showed that a HK intake increased the miR‐194 expression in the mouse kidney. The qPCR further demonstrated that a HK intake increased the miR‐194 transcription. Moreover, a HK intake decreased the expression of ITSN1. The role of miR‐194 in regulating ITSN1 expression is further confirmed by Luciferase Assay. Moreover, down‐regulation of endogenous miR‐194 by the antagomer increased ITSN1 protein expression in HEK cells. The whole‐cell recording and biotin labeling technique further showed that expression of miR‐194 increased ROMK channel activity in HEK cells transfected with GFP‐ROMK1, and effect was abolished by co‐expression of ITSN1. We conclude that miR‐194 regulates ROMK channel activity by modulating ITSN1 translation and that HK‐induced increase in miR‐194 is involved in mediating the effect of a HK intake on ROMK channel activity.