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Microarray Analysis of Potassium‐Induced Genes in the Mouse Kidney
Author(s) -
Jackson Cynthia Ann
Publication year - 2008
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.22.1_supplement.1158.27
Subject(s) - homeostasis , potassium , kidney , potassium channel , glucose homeostasis , biology , chemistry , medicine , endocrinology , microbiology and biotechnology , insulin , insulin resistance , organic chemistry
The kidney maintains potassium (K) homeostasis in the body by excreting the excess potassium intake rapidly and efficiently. In the process of excreting the excess K‐load, many genes are either activated or deactivated to achieve the goal of maintaining potassium homeostasis. In order to understand some these underlying renal mechanisms involved in K homeostasis, RNA was isolated from mice fed a control diet (1.1 % K, NK) and mice fed a high K diet (5% K, HK) for seven days. Transcriptional profiles of the kidneys from NK and HK mice were compared using mouse Affymetrix GeneChip 430 2.0. Relevant gene expressions were confirmed by real time RT‐PCR. Several genes relating to potassium homeostasis were detected. The genes for the potassium channels increased six‐fold in ROMK (KCNJ‐1), four fold in KCNK‐1 or TWIK‐1, decreased two fold in KCNK‐5 or TASK‐2. Gene expression also increased in other components coupled to potassium homeostasis, such as SGK‐1 (2.5 fold), AQP‐4 (3 fold), RGS‐2 (4 fold), IGF‐2 (9 fold), PRIP (4 fold), GBP3 (6 fold), and CDKN1c (2 fold). This analysis indicates that other physiological functions that are not directly associated with the potassium channel, such as G‐protein and aquaporin‐4 may be required to achieve potassium homeostasis. A more comprehensive analysis is needed.