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Enigmatic Roles of the Epithelial Sodium Channel (ENaC) in Articular Chondrocytes and Osteoblasts: Mechanotransduction, Sodium Transport or Extracellular Sodium Sensing?.

Editors

In: Kamkin A, Kiseleva I, editors.

Source

Mechanosensitivity in Cells and Tissues. Moscow: Academia; 2005.

Author information

1
Faculty of Veterinary Science, The University of Liverpool, Liverpool, L69 7ZJ, United Kingdom
2
Ludwig-Maximilians-University Munich, Faculty of Medicine, Institute of Anatomy, 80336 Munich, Germany
3
Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut, 06520-8026, United States of America
4
Laboratory of Developmental Biology, Department of Biochemistry and Molecular Biology, University of La Laguna, 38206 La Laguna, Tenerife, Spain

Excerpt

The mammalian MEC/DEG/ENaC gene superfamily encodes membrane proteins which are involved in diverse functions including acid sensing, maintenance of sodium homeostasis and transduction of mechanical stimuli and nociceptive pain. In the principal cells of the distal nephron amiloride sensitive ENaC activity represents the rate-limiting step for sodium reabsorption. Epithelial sodium channel (ENaC) subunits have also been found in articular chondrocytes and osteoblasts. In this article we discuss the enigmatic roles of ENaC in skeletal cells including articular chondrocytes and osteoblasts and review recent papers in which ENaC has been proposed to participate in skeletal mechanotransduction, sodium transport and extracellular sodium sensing.

Copyright © 2005, Academia Publishing House Ltd.

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