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Possible role of NF-kappaB in Bcl-X(L) protection against hydrogen peroxide-induced PC12 cell death

Jung-Hee Jang1, Young-Joon Surh

  • 1Laboratory of Biochemistry and Molecular Toxicology, College of Pharmacy, Seoul National University, Seoul, South Korea.

Redox Report : Communications in Free Radical Research
|February 22, 2005
PubMed

Insights

Bcl-X(L) protein protects against oxidative stress-induced apoptosis in PC12 cells. This protection involves the transcription factor NF-kappaB and increased heme oxygenase-1 levels.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Neuroscience

Background:

  • Bcl-X(L) is a mitochondrial protein that inhibits apoptosis.
  • The precise mechanisms underlying Bcl-X(L)'s anti-apoptotic function are not fully understood.
  • Oxidative stress, induced by hydrogen peroxide (H2O2), triggers cell death pathways.

Purpose of the Study:

  • To investigate the role of Bcl-X(L) in protecting cultured rat pheochromocytoma (PC12) cells against H2O2-induced oxidative death.
  • To explore the involvement of the transcription factor NF-kappaB in Bcl-X(L)-mediated protection.

Main Methods:

  • PC12 cells were exposed to H2O2 to induce apoptosis.
  • Apoptosis was assessed by DNA fragmentation and Bax to Bcl-X(L) ratio.
  • PC12 cells were stably transfected with the bcl-X(L) gene.
  • NF-kappaB transcriptional and DNA binding activities were measured.
  • NF-kappaB inhibitors were used to assess their effect on cell death.
  • Heme oxygenase-1 levels were analyzed in Bcl-X(L) overexpressing cells.

Main Results:

  • H2O2 induced apoptotic cell death in PC12 cells, characterized by DNA fragmentation and an increased Bax/Bcl-X(L) ratio.
  • Stable transfection with bcl-X(L) rescued PC12 cells from H2O2-induced apoptosis.
  • PC12 cells overexpressing Bcl-X(L) showed enhanced NF-kappaB transcriptional and DNA binding activities.
  • Inhibition of NF-kappaB aggravated H2O2-induced cell death.
  • Bcl-X(L) overexpression led to higher levels of heme oxygenase-1, suggesting enhanced protection against oxidative stress.

Conclusions:

  • Bcl-X(L) confers protection against oxidative death induced by H2O2 in PC12 cells.
  • The transcription factor NF-kappaB appears to play a significant role in Bcl-X(L)-mediated cytoprotection.
  • Increased heme oxygenase-1 expression may contribute to the anti-oxidative effects of Bcl-X(L).

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