| First Author | Goldschmidt I | Year | 2004 |
| Journal | Cell Physiol Biochem | Volume | 14 |
| Issue | 1-2 | Pages | 113-20 |
| PubMed ID | 14976412 | Mgi Jnum | J:105359 |
| Mgi Id | MGI:3614763 | Doi | 10.1159/000076932 |
| Citation | Goldschimdt I, et al. (2004) Kidney and colon electrolyte transport in CHIF knockout mice. Cell Physiol Biochem 14(1-2):113-20 |
| abstractText | Corticosteroid hormone induced factor (CHIF) is a small epithelial-specific protein regulated by aldosterone and K+ intake. It is a member of the FXYD family of single span transmembrane proteins involved in the regulation of ion transport. Recent data have suggested that CHIF interacts with the a subunit of the Na+-K+-ATPase and increases the pump's affinity to cell Na+. CHIF knockout (KO) mice have mild renal phenotype under low Na+ or high K+ diets. The present study further characterizes kidney electrolyte metabolism in CHIF KO mice and describes abnormalities in the colonic ion transport function. Kidney: KO mice were not compromised in salt and water balance under resting conditions. Fractional excretions (FE) of Na+ and K+ were normal and the animals had no deficit in the adaptation to low Na+ or high K+ intake. Glucocorticoid treatment did not unmask any difference. The effects of amiloride on Na+ absorption were not different at any treatment protocol. In contrast, FEK+ was reduced by 35% in KO mice under low Na+ intake. COLON: Amiloride inhibitable Na+ absorption was reduced in distal colon by 42%, 54% and 58% under control conditions, glucocorticoid treatment and low Na+ intake, respectively. Also, the cAMP dependent ion transport was significantly diminished. Forskolin induced equivalent short circuit current (I'SC) was reduced by 41%, 32% and 58%, under control conditions, high K+, and low Na+ intake, respectively. The present findings support a role of CHIF as an indirect modulator of several different ion transport mechanisms and are consistent with regulation of the Na+-K+-ATPase as the common denominator. |
