Acute hypoxia activates an ENaC-like channel in rat pheochromocytoma (PC12) cells

Yeon Ju Bae, Jae Cheal Yoo, Nammi Park, Dawon Kang, Jaehee Han, Eunmi Hwang, Jae Yong Park, Seong Geun Hong

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Cells can resist and even recover from stress induced by acute hypoxia, whereas chronic hypoxia often leads to irreversible damage and eventually death. Although little is known about the response(s) to acute hypoxia in neuronal cells, alterations in ion channel activity could be preferential. This study aimed to elucidate which channel type is involved in the response to acute hypoxia in rat pheochromocytomal (PC12) cells as a neuronal cell model. Using perfusing solution saturated with 95% N2 and 5% CO2, induction of cell hypoxia was confirmed based on increased intracellular Ca2+ with diminished oxygen content in the perfusate. During acute hypoxia, one channel type with a conductance of about 30 pS (2.5 pA at?80 mV) was activated within the first 2-3 min following onset of hypoxia and was long-lived for more than 300 ms with high open probability (Po, up to 0.8). This channel was permeable to Na+ ions, but not to K+, Ca+, and Cl- ions, and was sensitively blocked by amiloride (200 nM). These characteristics and behaviors were quite similar to those of epithelial sodium channel (ENaC). RT-PCR and Western blot analyses confirmed that ENaC channel was endogenously expressed in PC12 cells. Taken together, a 30-pS ENaC-like channel was activated in response to acute hypoxia in PC12 cells. This is the first evidence of an acute hypoxia-activated Na+ channel that can contribute to depolarization of the cell.

Original languageEnglish
Pages (from-to)57-64
Number of pages8
JournalKorean Journal of Physiology and Pharmacology
Volume17
Issue number1
DOIs
Publication statusPublished - 2013 Jan

Keywords

  • Acute hypoxia
  • Amiloride
  • Epithelial Na channel
  • PC12 Cells
  • Rats

ASJC Scopus subject areas

  • Physiology
  • Pharmacology

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