Parathyroid hormone and skeletal muscle cells

Abstract

Synthetized by the parathyroid glands, parathyroid hormone (PTH) is a single-chain, 84-amino acid polypeptide that controls calcium homeostasis by increasing serum levels, regulating calcium absorption in the small intestine (indirectly thanks to the action of calcitriol), renal reabsorption and removal from the bone matrix. It exerts its classical action mainly by interacting with PTH receptor type 1, a G protein-coupled receptor that is expressed in bone and kidney and activates different signaling pathways. Disorders of the parathyroid glands most commonly present with abnormal serum calcium concentrations: persistent high blood calcium levels are associated with hyperparathyroidism, whereas reduced blood calcium levels are associated with hypoparathyroidism. Both diseases are characterized by muscular dysfunction and myopathies. Even though numerous works suggest an effect of PTH on skeletal muscle, and PTH receptors have been identified in this tissue, knowledge of the cellular and molecular mechanisms of action of this hormone in skeletal muscle is very poor. It is hypothesized that skeletal muscle may be a target for PTH and that its receptors may mediate the effects of PTH. To support these hypotheses and obtain better and more specific understanding for future therapies, it needs to be established, using in vitro cellular models, whether PTH can affect skeletal muscle cell proliferation and differentiation.