Exploring the role of ghrelin peptides in sarcopenia development during aging
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Sarcopenia is a complex syndrome defined as the irreversible loss of skeletal muscle mass and functionality in aged individuals that results in frailty, mobility disorders, and loss of inde- pendence . The pathology is characterized by muscle atrophy and impaired muscle regenera- tion. The mechanisms involved in its development are not fully understood, although hormonal changes, inflammation, insulin resistance and nutritional deficiencies are surely involved in. In addition, we and other authors showed that aging affect progenitor myogenic cells, includingmesoangioblasts (adult vessel-associated stem cells)  unable to counteract sarcopenic pheno- type. Due to the increase of the elderly population, sarcopenia has an important social impact, greatly affecting the quality of life of aged people and impacting government health care costs. Therefore, therapeutic strategies aimed at preventing and/or counteracting sarcopenia are of pivotal importance.
Acylated and unacylated ghrelin (AG and UnAG, respectively) are circulating peptides codified by the ghrelin gene. By acting through its receptor GHSR1a, AG stimulates appetite, adiposity, a strong release of growth hormone (GH) and has a broad anti-inflammatory activ- ity. UnAG does not bind to GHSR1a however, similar to AG has a direct anti-atrophic effect on skeletal muscle .
Our preliminary results show that murine mesoangioblasts treated with recombinant UnAG or AG were able to differentiate spontaneously forming myotubes. In addition, in murine embry- onic stem cells and human mesodermal induced pluripotent stem cells subjected to myogenic dif- ferentiation, the presence of recombinant proteins resulted in improved myogenic commitment.
Taken together our results candidate AG and UnAG as potent myogenic inducers, able to modulate the gene expression profile in myogenic progenitors, affecting positively the muscle differentiation process.
This work was supported by grant CARIPLO Foundation #2015_0634.