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Overexpression of Insulin-Like Growth Factor-1 in the Heart is Coupled with Myocyte Proliferation in Transgenic Mice

Krzysztof Reiss, Wei Cheng, Andres Ferber, Jan Kajstura, Peng Li, Baosheng Li, Giorgio Olivetti, Charles J. Homcy, Renato Baserga and Piero Anversa
Proceedings of the National Academy of Sciences of the United States of America
Vol. 93, No. 16 (Aug. 6, 1996), pp. 8630-8635
Stable URL: http://www.jstor.org/stable/39915
Page Count: 6
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Overexpression of Insulin-Like Growth Factor-1 in the Heart is Coupled with Myocyte Proliferation in Transgenic Mice
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Abstract

Transgenic mice were generated in which the cDNA for the human insulin-like growth factor 1B (IGF-1B) was placed under the control of a rat α -myosin heavy chain promoter. In mice heterozygous for the transgene, IGF-1B mRNA was not detectable in the fetal heart at the end of gestation, was present in modest levels at 1 day after birth, and increased progressively with postnatal maturation, reaching a peak at 75 days. Myocytes isolated from transgenic mice secreted 1.15 ± 0.25 ng of IGF-1 per 106 cells per 24 hr versus 0.27 ± 0.10 ng in myocytes from homozygous wild-type littermates. The plasma level of IGF-1 increased 84% in transgenic mice. Heart weight was comparable in wild-type littermates and transgenic mice up to 45 days of age, but a 42%, 45%, 62%, and 51% increase was found at 75, 135, 210, and 300 days, respectively, after birth. At 45, 75, and 210 days, the number of myocytes in the heart was 21%, 31%, and 55% higher, respectively, in transgenic animals. In contrast, myocyte cell volume was comparable in transgenic and control mice at all ages. In conclusion, overexpression of IGF-1 in myocytes leads to cardiomegaly mediated by an increased number of cells in the heart.

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