| Physical activity protects and manages heart dysfunctions by modulating the mRNA expression profiles: A bioinformatics analysis |
| Paper ID : 1124-SSRC-13TH (R1) |
| Authors |
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Fatemeh Hajibabaie1, Navid Abedpoor2, Farzaneh Taghian *2 1Department of Physiology, Medicinal Plants Research Center, Isfahan (Khorasgan) Branch, Islamic Azad University, Isfahan, Iran 2Department of Sports Physiology, School of Sports Sciences, Isfahan (Khorasgan) Branch, Islamic Azad University, Isfahan, Iran |
| Abstract |
| Although the effects of exercise training on body performance are elucidated for everybody, evaluating the molecular signaling pathways and various mechanisms could suggest the mechanism of physical activity on the biochemical and physiological of the body. This study focuses on physical activity's influence on heart tissue function based on artificial intelligence analysis. Here, we selected the closest dataset to our aim with browsing in the Gene Expression Omnibus (GEO) server. These data were analyzed based on the Bioconductor package, Oligo, and Limma libraries in the R programming language. Moreover, the R programming language normalized microarray data based on the RMA platform. The microarray dataset analysis detected 980 significant genes considering P.value<.05 that 652 are upregulated and 328 downregulated in the physical activity conditions. Furthermore, a protein-protein interaction network was constructed with considering visualize parameters such as degree=10, betweenness centrality=0.1, and closeness centrality=0.3 in the Cytoscape 3.6.0 software and highlighted 55 genes with the highest degree and betweenness. In-silico analysis revealed that these 55 nodes significantly had the differential expression in biventricular tissue in physical activity. The data mining and bioinformatic analysis indicated that CASP3 with an upregulation pattern in the heart is defined as a proapoptotic and pro-inflammatory factor that is overexpressed in exercise training acutely. Based on these results, the overexpression of CASP3 by exercise led to increased adaptation in heart tissue's physiological levels via transient heart dysfunctions, myofibrillar damage. On the other hand, we found that CASP3 could be a candidate target for pharmaceutical design for heart damage therapeutic. |
| Keywords |
| Physical activity, CASP3 , Apoptosis, biventricular tissue |
| Status: Abstract Accepted (Oral Presentation) |
