Myocardial expression of a constitutively active alpha 1B-adrenergic receptor in transgenic mice induces cardiac hypertrophy.


Autoria(s): Milano, CA; Dolber, PC; Rockman, HA; Bond, RA; Venable, ME; Allen, LF; Lefkowitz, RJ
Data(s)

11/10/1994

Formato

10109 - 10113

Identificador

http://www.ncbi.nlm.nih.gov/pubmed/7937846

Proc Natl Acad Sci U S A, 1994, 91 (21), pp. 10109 - 10113

0027-8424

http://hdl.handle.net/10161/7840

Relação

Proc Natl Acad Sci U S A

10.1073/pnas.91.21.10109

Palavras-Chave #Animals #Atrial Natriuretic Factor #Blood Pressure #Body Weight #Cardiomegaly #Diglycerides #Gene Expression #Heart Ventricles #Humans #Mice #Mice, Transgenic #Mutagenesis, Site-Directed #Myocardium #Myosins #Organ Size #Point Mutation #Promoter Regions, Genetic #RNA, Messenger #Radioligand Assay #Receptors, Adrenergic, alpha-1 #Reference Values #Type C Phospholipases
Tipo

Journal Article

Cobertura

United States

Resumo

Transgenic mice were generated by using the alpha-myosin heavy chain promoter coupled to the coding sequence of a constitutively active mutant alpha 1B-adrenergic receptor (AR). These transgenic animals demonstrated cardiac-specific expression of this alpha 1-AR with resultant activation of phospholipase C as shown by increased myocardial diacylglycerol content. A phenotype consistent with cardiac hypertrophy developed in adult transgenic mice with increased heart/body weight ratios, myocyte cross-sectional areas, and ventricular atrial natriuretic factor mRNA levels relative to nontransgenic controls. These transgenic animals may provide insight into the biochemical triggers that induce hypertrophy in cardiac disease and serve as a convenient experimental model for studies of this condition.

Idioma(s)

ENG