Marked enhancement in myocardial function resulting from overexpression of a human β-adrenergic receptor gene

Carmelo A. Milano; Lee F. Allen; Paul C. Dolber; Thomas D. Johnson; Howard A. Rockman; Richard A. Bond; Robert J. Lefkowitz

doi:10.1016/S0022-5223(95)70384-5

Marked enhancement in myocardial function resulting from overexpression of a human β-adrenergic receptor gene

Carmelo A. Milano, Lee F. Allen, Paul C. Dolber, Thomas D. Johnson, Howard A. Rockman, Richard A. Bond, Robert J. Lefkowitz

Research output: Contribution to journal › Article › peer-review

18 Scopus citations

Abstract

Transgenic mice with intense cardiac expression of human β-adrenergic receptor gene were engineered and shown to display market improvements in baseline myocardial and left ventricular function. Heart/body weight ratios and histologic appearance were not found to be significantly altered, suggesting that receptor gene expression did not induce pathologic changes. Given the substantial reduction in β-adrenergic receptor density and result reduction in inotropic responsiveness observed in chronic heart failure, these finding represent a novel approach for increasing myocardial function with important clinical implications. (J THORAC CARDIOVASC SURG 1995;109:236-41).

Original language	English (US)
Pages (from-to)	236-241
Number of pages	6
Journal	The Journal of thoracic and cardiovascular surgery
Volume	109
Issue number	2
DOIs	https://doi.org/10.1016/S0022-5223(95)70384-5
State	Published - Feb 1995
Externally published	Yes

ASJC Scopus subject areas

Surgery
Pulmonary and Respiratory Medicine
Cardiology and Cardiovascular Medicine

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10.1016/S0022-5223(95)70384-5

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title = "Marked enhancement in myocardial function resulting from overexpression of a human β-adrenergic receptor gene",

abstract = "Transgenic mice with intense cardiac expression of human β-adrenergic receptor gene were engineered and shown to display market improvements in baseline myocardial and left ventricular function. Heart/body weight ratios and histologic appearance were not found to be significantly altered, suggesting that receptor gene expression did not induce pathologic changes. Given the substantial reduction in β-adrenergic receptor density and result reduction in inotropic responsiveness observed in chronic heart failure, these finding represent a novel approach for increasing myocardial function with important clinical implications. (J THORAC CARDIOVASC SURG 1995;109:236-41).",

author = "Milano, \{Carmelo A.\} and Allen, \{Lee F.\} and Dolber, \{Paul C.\} and Johnson, \{Thomas D.\} and Rockman, \{Howard A.\} and Bond, \{Richard A.\} and Lefkowitz, \{Robert J.\}",

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AU - Milano, Carmelo A.

AU - Allen, Lee F.

AU - Dolber, Paul C.

AU - Johnson, Thomas D.

AU - Rockman, Howard A.

AU - Bond, Richard A.

AU - Lefkowitz, Robert J.

PY - 1995/2

Y1 - 1995/2

N2 - Transgenic mice with intense cardiac expression of human β-adrenergic receptor gene were engineered and shown to display market improvements in baseline myocardial and left ventricular function. Heart/body weight ratios and histologic appearance were not found to be significantly altered, suggesting that receptor gene expression did not induce pathologic changes. Given the substantial reduction in β-adrenergic receptor density and result reduction in inotropic responsiveness observed in chronic heart failure, these finding represent a novel approach for increasing myocardial function with important clinical implications. (J THORAC CARDIOVASC SURG 1995;109:236-41).

AB - Transgenic mice with intense cardiac expression of human β-adrenergic receptor gene were engineered and shown to display market improvements in baseline myocardial and left ventricular function. Heart/body weight ratios and histologic appearance were not found to be significantly altered, suggesting that receptor gene expression did not induce pathologic changes. Given the substantial reduction in β-adrenergic receptor density and result reduction in inotropic responsiveness observed in chronic heart failure, these finding represent a novel approach for increasing myocardial function with important clinical implications. (J THORAC CARDIOVASC SURG 1995;109:236-41).

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Marked enhancement in myocardial function resulting from overexpression of a human β-adrenergic receptor gene

Abstract

ASJC Scopus subject areas

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