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Acta Physiologica Congress

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Acta Physiologica 2010; Volume 200, Supplement 681
Abstracts of the 61st National Congress of the Italian Physiological Society
9/15/2010-9/17/2010
Varese, Italy


NEURAL AGRIN ENHANCES THE REGENERATIVE POTENTIAL OF AGED HUMAN SKELETAL MYOBLASTS
Abstract number: O17

LORENZON1 P, LUIN1 E, FORMAGGIO2 E, FUMAGALLI2 G

1Dept Life Sciences and Centre for Neuroscience BRAIN, Trieste Univ., Trieste, Italy
2Dept Medicine and Public Health, Verona Univ., Verona, Italy

Neural agrin has been first described as a trophic factor released by the motor neuron due to its ability to promote the formation of the postsynaptic apparatus. Nowadays, experimental evidence demonstrates that the effect of neural agrin is not limited to the endplate region. Agrin causes remodelling of the skeletal muscle cell, improves the maturation of the excitation-contraction apparatus and governs the electrical properties of human myotubes.

The aim of the present work was to explore the trophic role of neural agrin on the regenerative potential of aged human myogenic cells. To do this, human myoblasts, derived from satellite cell isolated from aged donors, were cultured in the presence of 1 nM neural agrin. In this experimental condition, the proliferative capacity of aged myoblasts improved: they underwent a higher number of cell divisions before reaching the replicative senescence. The treatment with agrin did not alter the myogenic potential of aged human myoblasts: the percentage of desmin positive cells remained constant up to the terminally nondividing state. Agrin-treated myoblasts exhibited a fusion index and a number of nuclei per myotube similar to untreated cells. Preliminary experiments showed that myotubes generated by treated myoblasts exhibited a functional skeletal type excitation-contraction coupling mechanism.

Our results suggest that neural agrin enhances the proliferative potential of aged human satellite cells without affecting their myogenicity.

To cite this abstract, please use the following information:
Acta Physiologica 2010; Volume 200, Supplement 681 :O17

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