TY - JOUR
T1 - Role of intracellular Ca2+ in the expression of the amiloride-sensitive epithelial sodium channel
AU - Rao, U. Subrahmanyeswara
AU - Baker, James M.
AU - Pluznick, Jennifer L.
AU - Balachandran, Premalatha
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2004/1
Y1 - 2004/1
N2 - The amiloride-sensitive epithelial sodium channel (ENaC), a multimeric plasma membrane protein composed of α-, β-, and γ-ENaC subunits, mediates Na+ reabsorption in epithelial tissues, including the distal nephron, colon, lung, and secretory glands, and plays a critical role in pathophysiology of essential hypertension and cystic fibrosis (CF). The function of ENaC is tightly regulated by signals elicited by aldosterone, vasopressin, agents that increase intracellular cAMP levels, ions, ion channels, G-protein-coupled mechanisms, and cytoskeletal proteins. In this paper, the effects of Ca2+ on the expression of the human ENaC subunits expressed in human embryonic kidney cells (HEK-293 cells) were examined. Incubation of cells with increased extracellular Ca2+ and treatment of cells with A23187 and thapsigargin stimulated the expression of the monomeric ENaC subunits. Treatment of cells with Ca2+-chelating agents, EGTA and BAPTA-AM, reduced the levels of ENaC subunit expression. The pulse-chase experiments suggested that a rise in the intracellular Ca2+ increases the ENaC subunit expression. Immunoblot analysis using the anti-ubiquitin antibody indicated that ENaC undergoes ubiquitination. A correlation between the processes that regulate ENaC function with the intracellular Ca2+ was discussed.
AB - The amiloride-sensitive epithelial sodium channel (ENaC), a multimeric plasma membrane protein composed of α-, β-, and γ-ENaC subunits, mediates Na+ reabsorption in epithelial tissues, including the distal nephron, colon, lung, and secretory glands, and plays a critical role in pathophysiology of essential hypertension and cystic fibrosis (CF). The function of ENaC is tightly regulated by signals elicited by aldosterone, vasopressin, agents that increase intracellular cAMP levels, ions, ion channels, G-protein-coupled mechanisms, and cytoskeletal proteins. In this paper, the effects of Ca2+ on the expression of the human ENaC subunits expressed in human embryonic kidney cells (HEK-293 cells) were examined. Incubation of cells with increased extracellular Ca2+ and treatment of cells with A23187 and thapsigargin stimulated the expression of the monomeric ENaC subunits. Treatment of cells with Ca2+-chelating agents, EGTA and BAPTA-AM, reduced the levels of ENaC subunit expression. The pulse-chase experiments suggested that a rise in the intracellular Ca2+ increases the ENaC subunit expression. Immunoblot analysis using the anti-ubiquitin antibody indicated that ENaC undergoes ubiquitination. A correlation between the processes that regulate ENaC function with the intracellular Ca2+ was discussed.
KW - Amiloride-sensitive epithelial sodium channel
KW - Cystic fibrosis
KW - HEK-293 cells
KW - Intracellular Ca
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U2 - 10.1016/S0143-4160(03)00157-X
DO - 10.1016/S0143-4160(03)00157-X
M3 - Article
C2 - 14670368
AN - SCOPUS:0346728585
SN - 0143-4160
VL - 35
SP - 21
EP - 28
JO - Cell Calcium
JF - Cell Calcium
IS - 1
ER -