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| Title |
Aldehyde Dehydrogenase 2 Knockout Increases Ethanol-Induced Cardiac Depression: Role of Protein Phosphatases
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| Type of Resource |
still image
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| Date Created |
2009-05-13
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| Digital Origin |
born digtal
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| Rights Statement |
http://digital.uwyo.edu/copyright.htm
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| Keyword (topic) |
Cardiomyopathy
Acetaldehyde
cardiac hypertrophy
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| Series Title |
Undergrauate Research Day 2009
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| Creator(s) |
Byra, Emily
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| Contributor(s) |
Ren, Dr. Jun
Ma, Dr. Heng
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| Publisher |
University of Wyoming
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| Place of publication |
Laramie, Wyoming
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| Language |
eng
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| Summary |
Alcohol intake contributes to alcoholic cardiomyopathy characterized by cardiac hypertrophy and contractile dysfunction. Acetaldehyde, the first metabolic product of ethanol, has been marked as a major cause of alcoholic cardiomyopathy initiation and aldehyde dehydrogenase 2 (ALDH2) has been thought to play a key role in oxidizing this acetaldehyde, thus providing a cardioprotective effect. The aim of this study was to examine the effects of cardiac acetaldehyde exposure through the transgenic knockout of ALDH2 enzyme after alcohol ingestion and to observe the Akt signaling pathway. Mechanical properties of cardiomyocytes from ALDH2 KO mice were compared to C57 mice after ingestion of alcohol. Western Blot was used to observe expression of the Akt signaling pathway. The ethanol-induced effect was significantly increased in the ALDH2 KO group. Alcohol exposure prolonged TR90 without affecting TPS in wild type group. The ethanol-induced prolonged duration of relengthening was significantly enhanced in the ALDH2 KO group. Compared with wild type mice, the phosphorylation of Akt response to alcohol stress was markedly decreased in the ALDH2 KO group. Alcohol exposure significantly increased the levels of protein phosphatase 2A in wild type and in the ALDH2 KO group. These results suggest that ALDH2 is a trigger for the Akt pathway in response to alcoholinduced injury and the ALDH2 transgene has a cardioprotective effect against alcohol-induced cardiac depression through inhibition of protein phosphatases.
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| Notes |
From - Undergraduate Research Day 2009 - Celebration of Research - Abstracts
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