Training on Cancer for Medical Representatives of Pharma Company
Abstract
1. Alefia Kothambawala
Dr. Michael Conboy
Role of Individual Fibroblast Growth Factors in the Activation of Skeletal Muscle Cells
Introduction: As tissues degenerate with age, they cannot regenerate as easily as in the past. Muscle stem
cells (satellite cells) become unresponsive to injury and so must be triggered externally to proliferate, which we
hypothesize can be done using fibroblast growth factors (FGFs). FGFs are key players in the processes of cell
proliferation, cell differentiation, and morphogenetic events and are expressed widely in embryonic, fetal, and
adult life. Objective: We seek to determine whether quiescent satellite cells will activate and proliferate from
atypical FGF signaling (FGF-6 or FGF-19), thus propelling the cells out of the G0 phase of the cell cycle.
Methods: Cells used for these assays will be adult mouse muscle satellite cells that have yet to proliferate. We
will use an assay to determine which cells are proliferating by seeing if they take up bromodeoxyuridine (BrdU),
a thymine analog. Two controls will be set up: a positive control (F10+ 20% serum+ BFGE), and a negative
control (1% serum + basal medium), with FGF-2 and FGF-19 as experimental conditions. Also, the cells will be
stained with desmin, a protein that forms the intermediate filaments of muscle cells, to confirm whether they
are myogenic in origin. Results: The positive control had the greatest number of satellite cells that were
actively proliferating (61%), while the negative control had the least amount (32%). In addition, the FGF-2 and
FGF-19 conditions had 53% and 45% of cells that were proliferating respectively. Also, through statistical
analysis, we determined that our results were statistically significant, with little chance variation occurring
between samples. Conclusion: We conclude that FGF-2 and FGF-19 are potential activators of the muscle
regeneration machinery, stimulating satellite cells from the G0 phase and causing them to proliferate.
Acknowledgements: I would like to give my sincerest thanks to Dr. Michael Conboy for his instruction as well
as the use of his lab. In addition, I would like to thank Dr. Wendy Cousin for her kind support and involvement
despite her busy schedule. Lastly, I am grateful towards Prasana for serving as a guide through the details of
the experimental procedure.
Key Words: cell cycle, aging, sarcopenia