fibroblast growth factor (fgf-2) prevents human cardiac

Abstracts CONCLUSION:

In this pilot study there were no observable histological differences in human right atrial tissue from individuals at high- and low-risk for OSA. Further investigation would be required for more definitive results.

Canadian Cardiovascular Society (CCS) Oral THE HUMAN MYOCYTE Saturday, October 25, 2014

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myofibrotic phenotype. In contrast, FGF-2 treatment resulted in shorter cell extensions with a phenotype more consistent with quiescent fibroblasts. In addition, FGF-2 attenuated fibroblast-mediated matrix compaction relative to the TGF-b group. CONCLUSION: FGF-2 attenuates TGF- b1 mediated human cardiac fibroblast activation and restores ECM homeostasis and regulation. These data provide proof-of-concept evidence for FGF-2’s therapeutic potential in preventing adverse cardiac remodeling and subsequently heart failure.

Trainee Research Award Finalist e Basic Science 196 FIBROBLAST GROWTH FACTOR (FGF-2) PREVENTS HUMAN CARDIAC FIBROBLAST-MEDIATED EXTRACELLULAR MATRIX REMODELING DA Svystonyuk, JM Ngu, HE Mewhort, DG Guzzardi, BD Lipon, D Park, G Teng, DD Belke, PW Fedak Calgary, Alberta BACKGROUND: After myocardial injury, elevation of profibrotic cytokine transforming growth factor-b1 (TGF-b1) results in myofibroblast differentiation leading to matrix remodeling and progression of heart failure. Fibroblast growth factor (FGF-2) has the potential to antagonize TGF-b1’s profibrotic actions. In this study, we examine the effects of FGF-2 on human cardiac fibroblast mediated extracellular matrix remodeling. METHODS AND RESULTS: Human cardiac fibroblasts were isolated from atrial or ventricular heart biopsies and seeded into 3D collagen matrices. Myofibroblast activation was functionally assessed by the extent of matrix contraction. As compared to baseline myofibroblast activity, FGF-2 attenuated TGF-b1 mediated myofibroblast activation (1.06 versus 1.17, P