The vascular smooth muscle alpha-actin gene is reactivated during cardiac hypertrophy provoked by load
| Autor: | Michael D. Schneider, Lloyd H. Michael, Robert J. Schwartz, F. M. Black, S E Packer, Robert Roberts, Thomas G. Parker |
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| Rok vydání: | 1991 |
| Předmět: |
Male
Transcriptional Activation medicine.medical_specialty Vascular smooth muscle Cardiomegaly Biology Aortic Coarctation Muscle Smooth Vascular Muscle hypertrophy Fetus Genes jun Ventricular hypertrophy Internal medicine medicine Animals Myocyte RNA Messenger Actin Myogenesis Genes fos Skeletal muscle General Medicine medicine.disease Actins Rats medicine.anatomical_structure Endocrinology Gene Expression Regulation ITGA7 Research Article |
| Zdroj: | Journal of Clinical Investigation. 88:1581-1588 |
| ISSN: | 0021-9738 |
| DOI: | 10.1172/jci115470 |
| Popis: | Cardiac hypertrophy triggered by mechanical load possesses features in common with growth factor signal transduction. A hemodynamic load provokes rapid expression of the growth factor-inducible nuclear oncogene, c-fos, and certain peptide growth factors specifically stimulate the "fetal" cardiac genes associated with hypertrophy, even in the absence of load. These include the gene encoding vascular smooth muscle alpha-actin, the earliest alpha-actin expressed during cardiac myogenesis; however, it is not known whether reactivation of the smooth muscle alpha-actin gene occurs in ventricular hypertrophy. We therefore investigated myocardial expression of the smooth muscle alpha-actin gene after hemodynamic overload. Smooth muscle alpha-actin mRNA was discernible 24 h after coarctation and was persistently expressed for up to 30 d. In hypertrophied hearts, the prevalence of smooth muscle alpha-actin gene induction was 0.909, versus 0.545 for skeletal muscle alpha-actin (P less than 0.05). Ventricular mass after 2 d or more of aortic constriction was more highly correlated with smooth muscle alpha-actin gene activation (r = 0.852; P = 0.0001) than with skeletal muscle alpha-actin (r = 0.532; P = 0.009); P less than 0.0005 for the difference in the correlation coefficients. Thus, smooth muscle alpha-actin is a molecular marker of the presence and extent of pressure-overload hypertrophy, whose correlation with cardiac growth at least equals that of skeletal alpha-actin. Induction of smooth muscle alpha-actin was delayed and sustained after aortic constriction, whereas the nuclear oncogenes c-jun and junB were expressed rapidly and transiently, providing potential dimerization partners for transcriptional control by c-fos. |
| Databáze: | OpenAIRE |
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