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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Desai, K. Vranizan, K. Warrington, J. A. Bernstein, D. Nanevicz, T. Lee, E. K. Baker, A. J. Shah, N. Conklin, B. R. Fishman, G. I. Coward, P. Kwa, A. T. Cotte, N. Fidelman, N. Degtyarev, M. Y. Redfern, C. H. Salomonis, N. |
| Description | Author Affiliation: Redfern CH ( Gladstone Institute of Cardiovascular Disease and Gladstone Institute of Neurological Disease, Department of Medicine, University of California, San Francisco, CA 94141-9100, USA.); |
| Abstract | Cardiomyopathy is a major cause of morbidity and mortality. Ventricular conduction delay, as shown by prolonged deflections in the electrocardiogram caused by delayed ventricular contraction (wide QRS complex), is a common feature of cardiomyopathy and is associated with a poor prognosis. Although the G(i)-signaling pathway is up-regulated in certain cardiomyopathies, previous studies suggested this up-regulation was compensatory rather than a potential cause of the disease. Using the tetracycline transactivator system and a modified G(i)-coupled receptor (Ro1), we provide evidence that increased G(i) signaling in mice can result in a lethal cardiomyopathy associated with a wide QRS complex arrhythmia. Induced expression of Ro1 in adult mice resulted in a >90% mortality rate at 16 wk, whereas suppression of Ro1 expression after 8 wk protected mice from further mortality and allowed partial improvement in systolic function. Results of DNA-array analysis of over 6,000 genes from hearts expressing Ro1 are consistent with hyperactive G(i) signaling. DNA-array analysis also identified known markers of cardiomyopathy and hundreds of previously unknown potential diagnostic markers and therapeutic targets for this syndrome. Our system allows cardiomyopathy to be induced and reversed in adult mice, providing an unprecedented opportunity to dissect the role of G(i) signaling in causing cardiac pathology. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 9 |
| Volume Number | 97 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2000-05-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Cardiomyopathies Physiopathology Receptors, Opioid, Kappa Physiology Ventricular Function Animals Genetics Doxycycline Pharmacology Electrocardiography GTP-Binding Protein Alpha Subunits, Gi-Go Heart Mice Mice, Transgenic Myocardium Pathology Myosin Heavy Chains Signal Transduction Survival Analysis Tachycardia, Ventricular Tetracycline Resistance Drug Effects Virulence Factors, Bordetella 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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