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Am J Physiol Heart Circ Physiol 285: H1261-H1269, 2003. First published May 8, 2003; doi:10.1152/ajpheart.00108.2003
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Minimally invasive aortic banding in mice: effects of altered cardiomyocyte insulin signaling during pressure overload

Ping Hu,2 Dongfang Zhang,2 LeAnne Swenson,2,3 Gopa Chakrabarti,3,4 E. Dale Abel,3,4 and Sheldon E. Litwin1,2

1Division of Cardiology, Salt Lake City Veterans Affairs Medical Center, Salt Lake City 84148; and 2Division of Cardiology, 3Division of Endocrinology, Metabolism, and Diabetes, and 4Program in Human Molecular Biology and Genetics, The University of Utah, Salt Lake City, Utah 84132

Submitted 4 February 2003 ; accepted in final form 21 May 2003

We developed a minimally invasive method for producing left ventricular (LV) pressure overload in mice. With the use of this technique, we quickly and reproducibly banded the transverse aorta with low surgical morbidity and mortality. Minimally invasive transverse aortic banding (MTAB) acutely and chronically increased LV systolic pressure, increased heart weight-to-body weight ratio, and induced myocardial fibrosis. We used this technique to determine whether reduced insulin signaling in the heart altered the cardiac response to pressure overload. Mice with cardiac myocyte-restricted knockout of the insulin receptor (CIRKO) have smaller hearts than wild-type (WT) controls. Four weeks after MTAB, WT and CIRKO mice had comparably increased LV systolic pressure, increased cardiac mass, and induction of mRNA for {beta}-myosin heavy chain and atrial natriuretic factor. However, CIRKO hearts were more dilated, had depressed LV systolic function by echocardiography, and had greater interstitial fibrosis than WT mice. Expression of connective tissue growth factor was increased in banded CIRKO hearts compared with WT hearts. Thus lack of insulin signaling in the heart accelerates the transition to a more decompensated state during cardiac pressure overload. The use of the MTAB approach should facilitate the study of the pathophysiology and treatment of pressure-overload hypertrophy.

hypertrophy; contractility; fibrosis


Address for reprint requests and other correspondence: S. E. Litwin, Cardiovascular Div., Univ. of Utah Hospital, 50 N. Medical Dr., Salt Lake City, UT 84132 (E-mail: sheldon.litwin{at}hsc.utah.edu).




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