Ethanol increases TIEG2-MAO B cell death cascade in the prefrontal cortex of ethanol-preferring rats

Xiao Ming Ou, Chandra Johnson, Deyin Lu, Shakevia Johnson, Ian A. Paul, Mark C. Austin, Abiye H. Iyo, Jose Javier Miguel-Hidalgo, Jia Luo, Richard Bell, Matthew Grunewald, Junming Wang, Donald B. Sittman

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Brain cell loss has been reported in subjects with alcoholism. However, the molecular mechanisms are unclear. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and monoamine oxidase B (MAO B) reportedly play a role in cellular dysfunction with regards to ethanol exposure. We have recently reported that GAPDH protein expression was increased in the brains of rats fed with ethanol. Furthermore, GAPDH interacts with the transcriptional activator, transforming growth factor-beta-inducible early gene 2 (TIEG2), to augment TIEG2-mediated MAO B activation, resulting in neuronal cell damage due to ethanol exposure. The current study investigates whether the TIEG2-MAO B cascade is also active in the brains of rats fed with ethanol. Ten ethanol-preferring rats were fed with a liquid diet containing ethanol, with increasing amounts of ethanol up to a final concentration of 6.4% representing a final diet containing 36% of calories for 28 days. Ten control rats were fed the liquid diet without ethanol. The expression of TIEG2 protein, MAO B mRNA levels, MAO B catalytic activity, and the levels of anti-apoptotic protein Bcl 2 and apoptotic protein caspase 3 were determined in the prefrontal cortex of the rats. Ethanol significantly increased protein levels of TIEG2, active caspase 3, MAO B mRNA and enzyme activity, but significantly decreased Bcl 2 protein expression compared to control rats. In summary, ethanol increases the TIEG2-MAO B brain cell death cascade in rat brains, suggesting that the TIEG2-MAO B pathway is a novel pathway for brain cell damage resulting from ethanol exposure, and may contribute to chronic alcohol-induced brain damage.

Original languageEnglish
Pages (from-to)511-518
Number of pages8
JournalNeurotoxicity Research
Volume19
Issue number4
DOIs
StatePublished - May 2011

Fingerprint

Monoamine Oxidase
Cell death
Prefrontal Cortex
Rats
B-Lymphocytes
Cell Death
Ethanol
Brain
Glyceraldehyde-3-Phosphate Dehydrogenases
Nutrition
Rat control
Diet
Proteins
Caspase 3
Cells
Messenger RNA
Apoptosis Regulatory Proteins
Brain Death
Enzyme activity
Liquids

Keywords

  • Active caspase 3
  • Alcoholism
  • Apoptosis
  • Bcl 2
  • Cell death pathway
  • Ethanol-preferring rats
  • Monoamine oxidase B
  • Transforming growth factor-beta- inducible early gene 2

ASJC Scopus subject areas

  • Neuroscience(all)
  • Toxicology

Cite this

Ou, X. M., Johnson, C., Lu, D., Johnson, S., Paul, I. A., Austin, M. C., ... Sittman, D. B. (2011). Ethanol increases TIEG2-MAO B cell death cascade in the prefrontal cortex of ethanol-preferring rats. Neurotoxicity Research, 19(4), 511-518. https://doi.org/10.1007/s12640-010-9164-4

Ethanol increases TIEG2-MAO B cell death cascade in the prefrontal cortex of ethanol-preferring rats. / Ou, Xiao Ming; Johnson, Chandra; Lu, Deyin; Johnson, Shakevia; Paul, Ian A.; Austin, Mark C.; Iyo, Abiye H.; Miguel-Hidalgo, Jose Javier; Luo, Jia; Bell, Richard; Grunewald, Matthew; Wang, Junming; Sittman, Donald B.

In: Neurotoxicity Research, Vol. 19, No. 4, 05.2011, p. 511-518.

Research output: Contribution to journalArticle

Ou, XM, Johnson, C, Lu, D, Johnson, S, Paul, IA, Austin, MC, Iyo, AH, Miguel-Hidalgo, JJ, Luo, J, Bell, R, Grunewald, M, Wang, J & Sittman, DB 2011, 'Ethanol increases TIEG2-MAO B cell death cascade in the prefrontal cortex of ethanol-preferring rats', Neurotoxicity Research, vol. 19, no. 4, pp. 511-518. https://doi.org/10.1007/s12640-010-9164-4
Ou, Xiao Ming ; Johnson, Chandra ; Lu, Deyin ; Johnson, Shakevia ; Paul, Ian A. ; Austin, Mark C. ; Iyo, Abiye H. ; Miguel-Hidalgo, Jose Javier ; Luo, Jia ; Bell, Richard ; Grunewald, Matthew ; Wang, Junming ; Sittman, Donald B. / Ethanol increases TIEG2-MAO B cell death cascade in the prefrontal cortex of ethanol-preferring rats. In: Neurotoxicity Research. 2011 ; Vol. 19, No. 4. pp. 511-518.
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abstract = "Brain cell loss has been reported in subjects with alcoholism. However, the molecular mechanisms are unclear. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and monoamine oxidase B (MAO B) reportedly play a role in cellular dysfunction with regards to ethanol exposure. We have recently reported that GAPDH protein expression was increased in the brains of rats fed with ethanol. Furthermore, GAPDH interacts with the transcriptional activator, transforming growth factor-beta-inducible early gene 2 (TIEG2), to augment TIEG2-mediated MAO B activation, resulting in neuronal cell damage due to ethanol exposure. The current study investigates whether the TIEG2-MAO B cascade is also active in the brains of rats fed with ethanol. Ten ethanol-preferring rats were fed with a liquid diet containing ethanol, with increasing amounts of ethanol up to a final concentration of 6.4{\%} representing a final diet containing 36{\%} of calories for 28 days. Ten control rats were fed the liquid diet without ethanol. The expression of TIEG2 protein, MAO B mRNA levels, MAO B catalytic activity, and the levels of anti-apoptotic protein Bcl 2 and apoptotic protein caspase 3 were determined in the prefrontal cortex of the rats. Ethanol significantly increased protein levels of TIEG2, active caspase 3, MAO B mRNA and enzyme activity, but significantly decreased Bcl 2 protein expression compared to control rats. In summary, ethanol increases the TIEG2-MAO B brain cell death cascade in rat brains, suggesting that the TIEG2-MAO B pathway is a novel pathway for brain cell damage resulting from ethanol exposure, and may contribute to chronic alcohol-induced brain damage.",
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