C. Capurro et al., CELLULAR-LOCALIZATION AND REGULATION OF CHIF IN KIDNEY AND COLON, American journal of physiology. Cell physiology, 40(3), 1996, pp. 753-762
Channel inducing factor (CHIF) is a novel cDNA recently cloned from a
rat distal colon cDNA library of dexamethasone-treated animals. While
its expression in Xenopus oocytes evokes a potassium channel activity
similar to that induced by Isk. (minK), its cellular role is not clear
. CHIF exhibits significant homologies with proteins that are putative
ly regulatory (phospholemman, gamma-subunit of Na+-K+-ATPase, Mat-8) w
hile it differs from the small-conductance potassium channel Isk. We h
ave studied the tissue specificity of CHIF expression in rat by in sit
u hybridization. CHIF is selectively present in the distal parts of th
e nephron (medullary and papillary collecting ducts and end portions o
f cortical collecting tubule) and in the epithelial cells of the dista
l colon. No expression of CHIF was found in renal proximal tubule, loo
p of Henle and distal tubule, proximal colon, small intestine, lung, c
horoid plexus, salivary glands, or brain. To gain some insight into CH
IF function, we have investigated, using in situ hybridization and rib
onuclease protection assay, whether CHIF mRNA expression could be alte
red in some situations. In the distal colon, corticosteroid hormones,
sodium restriction, low-potassium diet, and metabolic acidosis signifi
cantly increased CHIF mRNA expression. In the kidney, metabolic acidos
is was the only condition that showed an increase in CHIF mRNA express
ion. Some of these treatments also altered the expression of the colon
ic H+-K+-ATPase mRNA. In summary, CHIF mRNA is selectively expressed i
n the medullary collecting duct of the kidney and in the epithelium of
the distal colon; its expression varies differently in these two targ
et tissues after alterations in corticosteroid status, potassium deple
tion, and metabolic acidosis. The precise cell-specific functions of C
HIF remain to be established.