Overexpression of Kir2.3 in PC12 cells resists rotenone-induced neurotoxicity associated with PKC signaling pathway

Gang Wang, Jie Zeng, Cheng Yu Shen, Zhi Quan Wang, Sheng Di Chen

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

Parkinson's disease (PD) can be triggered by genetic or environmental factors. Although the precise etiopathogenesis of the disease remains unknown, recent studies focusing on the K+ channel gene have uncovered the dysfunctions in various K+ channels (e.g., Kir2, Kv, KATP, and SKCa) that are involved in the pathological mechanisms underlying PD. Here we show that Kir2.3 overexpression can protect against rotenone-induced apoptosis in cell models in the neurodegenerative process, suggesting Kir2.3's general neuroprotective function. The protection of Kir2.3 against neurodegeneration may be associated with the protein kinase C (PKC) pathway, as PKC is downregulated by Kir2.3 overexpression and the PKC activator can reduce the protective effect of Kir2.3. Our studies provide an entry point for understanding the novel roles of Kir2.3 in cell models of PD, and they offer clues for the common mechanisms underlying different neurodegenerative conditions.

Original languageEnglish (US)
Pages (from-to)204-209
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume374
Issue number2
DOIs
StatePublished - Sep 19 2008

Keywords

  • Inwardly rectifying potassium channel
  • Parkinson's disease
  • Protein kinase C
  • Rotenone

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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