How Ghrelin Modulates Muscle-to-Fat Differentiation in Mesenchymal Progenitor Cells

Sarcopenia is a progressive skeletal muscle disorder that causes gradual decline of skeletal muscle mass and strength. Various factors contribute to this decline, including reduced physical activity, hormonal fluctuations, oxidative stress, and nutritional decisions. Despite these known influences, the precise mechanisms driving muscle deterioration in sarcopenic individuals remain elusive. Ghrelin has been used as a therapeutic for treating sarcopenia, given its role in reducing muscle wasting and increasing muscle strength and lean body mass. However, research on the role of ghrelin’s receptor, GHSR-1a, in mesenchymal progenitor cells (MPCs) remains limited, despite evidence of ghrelin signaling impacting muscle and fat differentiation. In this study, we aimed to elucidate the pathogenic effects of ghrelin on muscle-to-fat differentiation in MPCs. We investigated the influence of human recombinant ghrelin on myocyte and adipocyte differentiation while employing CRISPR-Cas9 technology to delete GHSR-1a from MPCs. Surprisingly, we discovered the presence of GHSR-la in MPCs, a novel finding not previously analyzed. Furthermore, our results indicate that ghrelin influences the balance between muscle and fat differentiation in MPCs, while deletion of GHSR-1a leads to abnormal cell growth effects. These findings shed light on the complex interplay between ghrelin signaling and muscle homeostasis, providing valuable insights for finding out more about the complex mechanisms that cause the onset of sarcopenia. 

For more information: mewoodbu@eckerd.edu

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