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Am J Physiol Cell Physiol (September 28, 2005). doi:10.1152/ajpcell.00210.2005
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Submitted on May 2, 2005
Accepted on September 22, 2005

ENaC PROTEINS ARE REQUIRED FOR NGF-INDUCED NEURITE GROWTH

Heather A Drummond1*, Marise M Furtado1, Samuel Myers1, Samira Grifoni1, Kimberly A Parker1, Angela Hoover1, and David E Stec1

1 Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA

* To whom correspondence should be addressed. E-mail: hdrummond{at}physiology.umsmed.edu.

Neurite growth is required for nervous system development and repair. Multiple signals, including neurotrophic factors and intact mechanosensing mechanisms, interact to regulate neurite growth. Degenerin/Epithelial Na+ Channel (DEG/ENaC) proteins have been identified as putative mechanosensors in sensory neurons. Recently, others have shown the neurotrophic factor Nerve Growth Factor (NGF), stimulates expression of Acid-Sensing Ion Channel (ASIC) molecules, members of the DEG/ENaC. However, it is unknown if NGF regulates ENaC expression or if ENaC expression is required for neurite formation. Therefore, the aims of this study are to determine if ENaC expression is 1) regulated by NGF and 2) required for NGF-induced neurite growth in PC12 cells. We found NGF induced expression of {beta} and {gamma}, but not {alpha}ENaC. Tyrosine kinase A (TrkA) receptor blockade abolished NGF-induced {beta} and {gamma}ENaC expression and neurite formation. Disruption of ENaC expression using 1) pharmacological blockade with benzamil, a specific ENaC inhibitor, 2) siRNA and 3) dominant-negative ENaC molecules, inhibited NGF-induced neurite formation. These data indicate NGF-TrkA regulation of ENaC expression may be required for neurite growth and may suggest a novel role for DEG/ENaC proteins in neuronal remodeling and differentiation.




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