GENE EXPRESSION PROFILE INDUCED BY PHYSICAL EXERCISE IN RATS
Abstract number: P-W-623
Giusti1 B., Rossi1 L., Lapini1 I., Magi1 A., Capalbo1 A., Boddi1 M., Abbate1 R., Marini2 M., Samaya3 M., Vecsteinas4 A.
11Department of Medical and Surgical Critical Care, University of Florence, Florence 22General Istology and Embriology Institute, University of Bologna, Bologna 33Department of Medicine, University of Milan 44Center of Sport Medicine, Don C.Gnocchi Foundation, Milan, Italy
How-to-cite Giusti B, Rossi L, Lapini I, Magi A, Capalbo A, Boddi M, Abbate R, Marini M, Samaya M, Vecsteinas A. GENE EXPRESSION PROFILE INDUCED BY PHYSICAL EXERCISE IN RATS. J Thromb Haemost 2007; 5 Supplement 2: P-W-623
Abstract
Introduction: Physical exercise training is a known protective factor against cardiovascular morbidity and mortality. Nevertheless, the underlying specific molecular mechanisms still remain unexplored.In this study we investigated the gene expression profile induced by moderate exercise training on left ventricle (LV) obtained from heart of exercise-trained (n=10) and sedentary control (n=10) rats.
Methods: Rats in the training group exercised on a treadmill running at 20 m/min and 0-degree gradient for 1 h/day, 7 days/week, for 11 weeks. We used Affymetrix technology to identify LV gene expression profile in response to exercise (230 2.0 GeneChip rat genome array).
Results: Of the 31,000 probe sets represented on the GeneChip, after data processing and application of the filtering criteria, the average of analyzable features numbered 14,911. By using the Significance Analysis of Microarray (SAM) method to assess the expression of the 14,911 called transcripts we observed 11 transcripts (9 genes) differentially expressed in left ventricle hearts of exercise-trained animals with respect to sedentary controls. The genes that we found differentially expressed are involved in several biological processes. In particular, we pointed our attention in validating the up-regulation of four genes:
Caveolin 3 (Cav-3), a structural component of cardiac caveolae, critical for normal muscle function;
Enolase 3 beta (Eno3), that has been observed to confer positive regulation by hypoxia and was observed to increase after race in athletes;
Egl nine homolog 1 (Egln1), an important regulator of HIF-1a during hypoxia;
Cystatin C (Cst3), one of the most important extracellular inhibitors of cysteine proteases.
Conclusions: Our data may contribute to the comprehension of the molecular mechanisms responsible for the cardiovascular protective role of moderate physical exercise training. Further validation and functional studies are required in order to better evaluate the role of the genes emerged from the microarray analysis.
