NDLI: Disruption of type 5 adenylyl cyclase gene preserves cardiac function against pressure overload.

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Disruption of type 5 adenylyl cyclase gene preserves cardiac function against pressure overload.

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Disruption of type 5 adenylyl cyclase gene preserves cardiac function against pressure overload.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Vatner, Dorothy E. Okumura, Satoshi Takagi, Gen Liu, Jing Hong, Chull Lee, Ming-chih Vatner, Stephen F. Kawabe, Jun-ichi Sadoshima, Junichi Yang, Guiping Ishikawa, Yoshihiro
Description	Author Affiliation: Okumura S ( Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine and Department of Medicine, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark, NJ 07101-1709, USA.);
Abstract	The sympathetic nervous system is designed to respond to stress. Adenylyl cyclase (AC) is the keystone of sympathetic transmission, yet its role in response to acute overload in the heart or in the pathogenesis of heart failure is controversial. We examined the effects of pressure overload, induced by thoracic aortic banding, in mice in which type 5 AC, a major cardiac AC isoform, was disrupted (AC5-/-). Left ventricular weight/tibial length ratio (LVW/TL) was not different between the WT and AC5-/- at baseline and increased progressively and similarly in both groups at 1 and 3 wk after aortic banding. However, LV ejection fraction (LVEF) fell in WT at 3 wk after banding (from 70 +/- 2.8 to 57 +/- 3.9%, P < 0.05), and this decrease was associated with LV dilatation, indicating incipient cardiac failure. In contrast, AC5-/- mice did not exhibit a fall in LVEF from 74 +/- 2.2%. The number of apoptotic myocytes was similar at baseline, but it increased roughly 4-fold in WT at both 1 and 3 wk after banding, and significantly less, P < 0.05, in AC5-/-. Importantly, the increase in apoptosis occurred before the decline in LVEF in WT. The protective mechanism seems to involve Bcl-2, which was up-regulated significantly more in AC5-/- mice with pressure overload. Our findings suggest that limiting type 5 AC plays a protective role in response to pressure overload and the development of heart failure, potentially through limiting the incidence of myocardial apoptosis.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	17
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Adenylate Cyclase Genetics Heart Physiology Hypertension Enzymology Physiopathology Isoenzymes Deficiency Animals Apoptosis Cardiomegaly Etiology Disease Models, Animal Heart Failure Pathology Prevention & Control Mice Mice, Inbred C57BL Mice, Knockout Myocardium Cytology Proto-Oncogene Proteins C-bcl-2 Metabolism Signal Transduction Ventricular Function, Left Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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