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Estrogen's Role In Preventing Female Cardiac Disease

Date:
March 25, 2002
Source:
Cornell University
Summary:
The role of the hormone estrogen in protecting the female heart from enlargement and ultimate failure has been partly explained by studies with genetically engineered mice, according to researchers at Cornell and Vanderbilt universities.
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ITHACA, N.Y. -- The role of the hormone estrogen in protecting the female heart from enlargement and ultimate failure has been partly explained by studies with genetically engineered mice, according to researchers at Cornell and Vanderbilt universities.

Authors of the report in the latest issue of Nature ( March 21, 2002), "Oestrogen protects FKBP12.6 mice from cardiac hypertrophy," used the newly developed mouse "model" for an enlarged heart muscle to help explain estrogen's important role in preventing female cardiac hypertrophy -- extreme stress on the heart that is an early sign of congestive heart failure. However, the researchers say, much more research is needed into the complex causes of heart-muscle enlargement, a condition that leads to cardiac hypertrophy.

But results of the mouse studies, they say, are clear:

o Among mice genetically engineered for a predisposition to an enlarged heart muscle, male mice develop early signs of cardiac hypertrophy similar to the potentially fatal human condition, whereas similarly engineered female transgenic mice do not.

o Unless, that is, the female mice are treated with a drug to block natural estrogen production. By being unable to produce estrogen, the female mice had the same kind of cardiac hypertrophy as did the male mice -- indicating that estrogen production protects the females but not the males.

Referring to recent evaluations of estrogen replacement therapy for postmenopausal women, Michael Kotlikoff, professor and chair of clinical sciences at Cornell, says: "This finding correlates well with epidemiological data indicating an increase in the incidence of cardiomegaly (enlargement of the heart) in women after menopause. We are hopeful that these mice will provide insight to the processes leading to cardiac enlargement and the role that estrogen plays in ameliorating this process."

In addition to Kotlikoff, whose laboratory in the College of Veterinary Medicine at Cornell studies calcium channel signaling in muscle cells, authors of the Nature report include: Vanderbilt researchers Sidney Fleischer, Dong-Sheng Cheng, Julio A. Copello, Loice H. Jeyakumar, Tadashi Inagaml and Mark A. Magnuson; Mei Lin Collier of the University of Pennsylvania School of Veterinary Medicine; and Yong-Xiao Wang, Guang-Ju Ji, Ke-Yu Deng and Hong-Bo Xin of Cornell.

Now an assistant professor of biomedical sciences in Cornell's veterinary college, Xin was a postdoctoral researcher in Vanderbilt's Department of Biological Sciences when he developed the so-called knock-out mouse (or null mouse) that lacks the gene to produce the binding protein FKBP12.6. The protein is associated with receptors in heart muscle cells that signal for the contraction of muscle cells when calcium ions pass through channels, causing the heart to pump blood.

The Cornell-Vanderbilt mouse studies show for the first time how FKBP12.6 regulates the release of calcium in muscle-cell signaling, and also suggested that estrogen can protect mice -- and perhaps humans, too -- from the consequences of poorly regulated calcium release.

"When we examined cal


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Materials provided by Cornell University. Note: Content may be edited for style and length.


Cite This Page:

Cornell University. "Estrogen's Role In Preventing Female Cardiac Disease." ScienceDaily. ScienceDaily, 25 March 2002. <www.sciencedaily.com/releases/2002/03/020325080342.htm>.
Cornell University. (2002, March 25). Estrogen's Role In Preventing Female Cardiac Disease. ScienceDaily. Retrieved July 18, 2024 from www.sciencedaily.com/releases/2002/03/020325080342.htm
Cornell University. "Estrogen's Role In Preventing Female Cardiac Disease." ScienceDaily. www.sciencedaily.com/releases/2002/03/020325080342.htm (accessed July 18, 2024).

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