Minimally invasive aortic banding in mice: effects of altered cardiomyocyte insulin signaling during pressure overload

Hu, Ping; Zhang, Dongfang; Swenson, LeAnne; Chakrabarti, Gopa; Abel, E. Dale; Litwin, Sheldon E.

doi:10.1152/ajpheart.00108.2003

Cited by 245Cardiac Fibrosis and RemodelingCardiovascular Function and Risk FactorsCardiomyopathy and Myosin Studies

Minimally invasive aortic banding in mice: effects of altered cardiomyocyte insulin signaling during pressure overload

Hu, Ping, Zhang, Dongfang, Swenson, LeAnne, Chakrabarti, Gopa, Abel, E. Dale, Litwin, Sheldon E.·2003·American Journal of Physiology-Heart and Circulatory Physiology

DOI 10.1152/ajpheart.00108.2003

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Abstract

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 β-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.

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Insulin receptor-deficient hearts have increased susceptibility to injury when exposed to hypertrophic stimuli such as pressure overload and chronic adrenergic stimulation with isoproterenol.
“Insulin receptor-deficient hearts also have increased susceptibility to injury when exposed to hypertrophic stimuli such as pressure overload and chronic adrenergic stimulation with isoproterenol (150, 231).”
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Authors: Hu, P., Zhang, D., Swenson, L., Chakrabarti, G., Abel, E. D., & Litwin, S. E.
Affiliations: University of Utah (US)
ORCID: Zhang, Dongfang
Abel, E. Dale
Litwin, Sheldon E.
Venue: American Journal of Physiology-Heart and Circulatory Physiology
Publisher: American Physiological Society
Published: 2003-09
Volume: 285
Issue: 3
Pages: H1261-H1269
ISSN: 0363-6135 (ISSN-L)
1522-1539
DOI: 10.1152/ajpheart.00108.2003
OpenAlex: W2153616813
Cited by: 245
References: 44
Citations by year: 2026: 6 · 2025: 8 · 2024: 8 · 2023: 6 · 2022: 10 · 2021: 11 · 2020: 8 · 2019: 9 · 2018: 8 · 2017: 14 · 2016: 10 · 2015: 16 · 2014: 10 · 2013: 17 · 2012: 16
FWCI: 4.39
Type: journal article
Language: en
Open access: closed
Locations: American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5r03dk058073-03)
U.S. Public Health Service (U01-70525)
National Heart, Lung, and Blood Institute (T32-HL-7576, HL-52338-06, P50HL052338, T32HL007576)
National Institute of Diabetes and Digestive and Kidney Diseases (DK58073, R01DK092065)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
Keywords: left ventricular pressure overload, cardiac hypertrophy, myocardial fibrosis, connective tissue growth factor, beta-myosin heavy chain, atrial natriuretic peptide, cardiac remodeling, heart failure
MeSH terms: Animals, Aorta, Blood Pressure, Disease Models, Animal, Fibrosis, Insulin, Male, Mice, Inbred C57BL, Myocardial Contraction, Signal Transduction, Hypertrophy, Left Ventricular, Ventricular Pressure, Myocytes, Cardiac, Mice

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Minimally invasive aortic banding in mice: effects of altered cardiomyocyte insulin signaling during pressure overload

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