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| Title |
17beta-Estradiol supplementation attenuates cardiomyocyte contractile dysfunction via activation of AMP-activated protein kinase (AMPK) in ovariectomized mice
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| Type of Resource |
still image
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| Date Created |
2009-05-14
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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) |
Cardiovascular disease
AMPactivated protein kinase (AMPK)
7beta-Estradiol
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| Series Title |
Undergrauate Research Day 2009
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| Creator(s) |
Huff, Anna
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| Contributor(s) |
Ren, Dr. Jun
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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 |
Cardiovascular disease is significantly lower in premenopausal women than males or postmenopausal women, attributed to the protective role of estrogen, in addition to reduced insulin sensitivity and increased risk of type 2 diabetes associated with diabetic cardiomyopathy. AMPactivated protein kinase (AMPK) increases energy supply by increasing glucose transport and free fatty acid utilization. AMPK activation by estrogen was recently observed in C2C12 myotubes and rat skeletal muscle in vitro. However, little is known about how estrogen affects AMPK signaling in the heart. The major aim of this study is to observe the effects of 17beta-Estradiol supplementation on ventricular myocyte contractile function and AMPK activation. Female C57 mice were subjected to bilateral ovariectomy (Ovx) or sham operation (sham). A subgroup of Ovx mice were given 17beta- Estradiol supplement (IP, 40µg/kg/day) for 6 weeks. Mechanical and intracellular Ca2+ properties were evaluated, including peak shortening (PS), time to PS (TPS), time to 90% relengthening (TR(90)), maximal velocity of shortening/relengthening (+/-dL/dt). Levels of AMPK, pAMPK, Akt, pAkt, pACC and pAS160 were assessed by Western blot. Ovx decreased PS and ±dL/dt, TR(90) with the exception of TPS. Interestingly, 17beta-Estradiol supplementation restored the depression in PS and ±dL/dt but failed to reverse in TR90, which was associated with prolongation in the intracellular calcium decay rate. Western blot results showed that Ovx did not alter the levels of total Akt and AMPK, but ablated the activation of both. These alterations in protein expression were restored by 17beta-Estradiol. The expression levels of pACC and pAS160 were found slightly depressed in Ovx mice but not significant. These data suggest that 17beta-Estradiol supplementation attenuates the abnormalities of mechanical and protein functions in ventricular myocytes caused by estrogen deficiency and the crosstalk between the estrogen receptor and AMPK signaling pathways may play an important role.
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| Notes |
From - Undergraduate Research Day 2009 - Celebration of Research - Abstracts
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