Publication Date:
1994-04-22
Description:
Transgenic mice were created with cardiac-specific overexpression of the beta 2-adrenergic receptor. This resulted in increased basal myocardial adenylyl cyclase activity, enhanced atrial contractility, and increased left ventricular function in vivo; these parameters at baseline in the transgenic animals were equal to those observed in control animals maximally stimulated with isoproterenol. These results illustrate a useful approach for studying the effect of gene expression on cardiac contractility. Because chronic heart failure in humans is accompanied by a reduction in the number of myocardial beta-adrenergic receptors and in inotropic responsiveness, these results suggest a potential gene therapy approach to this disease state.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Milano, C A -- Allen, L F -- Rockman, H A -- Dolber, P C -- McMinn, T R -- Chien, K R -- Johnson, T D -- Bond, R A -- Lefkowitz, R J -- 5F32-CA09350/CA/NCI NIH HHS/ -- HL-16037/HL/NHLBI NIH HHS/ -- HL-18468/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Apr 22;264(5158):582-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8160017" target="_blank"〉PubMed〈/a〉
Keywords:
Adenylyl Cyclases/*metabolism
;
Animals
;
Gene Transfer Techniques
;
Genetic Therapy
;
Heart Failure/physiopathology/therapy
;
Heart Rate
;
Humans
;
Isoproterenol/pharmacology
;
Mice
;
Mice, Transgenic
;
*Myocardial Contraction
;
Myocardium/*metabolism
;
Myosins/genetics
;
Phenotype
;
Promoter Regions, Genetic
;
Receptors, Adrenergic, beta/biosynthesis/*genetics/physiology
;
*Ventricular Function, Left
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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