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Quantitative responses of the mouse heart to pregnancy
Author(s) -
Chung Eunhee,
Leinwand Leslie A.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.969.7
Subject(s) - medicine , endocrinology , pregnancy , muscle hypertrophy , cardiac function curve , gestation , pressure overload , volume overload , heart failure , cardiac hypertrophy , biology , genetics
The heart changes its structure and function in response to various stimuli. Pathological stimuli initially activate an adaptive increase in mass, but may lead to heart failure. In contrast, cardiac hypertrophy induced by physiological stimuli, such as exercise, maintains or even enhances contractile function. A relatively under‐studied cardiac hypertrophic stimulus is pregnancy which is associated with altered estrogen levels and a prolonged cardiac volume overload. The objective of this study was to test the hypotheses that pregnancy could cause unique changes in function and signaling molecules compared to exiting other models of physiologic hypertrophy. Two‐to‐three month old virgin female C57/Bl6 mice were divided into non‐pregnant (NP), 10 to 13 days gestation (MP), and 18‐19 days gestation (LP). MP and LP have significant increases heart weight compared to NP. Fractional shortening (FS%) was significantly decreased in LP compared to NP and MP. We measured molecules in the PI3K pathway which have been implicated in exercise. The ratio of ph‐Akt to Akt and ph‐GSK3β to GSK3β were significantly increased in MP but returned to the NP level in LP. These results suggest that the PI3K pathway is activated in the early stage of pregnancy. We conclude that pregnancy‐induced cardiac hypertrophy is similar to but also distinct from exercise hypertrophy since systolic function (FS%) significantly decreased in LP.