Role of Cyclic AMP and Its Relationship to Parathyroid Hormone Response in an In vitro Model of Chondrogenesis.

摘要

Although previous studies have established cartilage as a target tissue for parathyroid hormone (PTH), it is not clear how the state of chondrocyte maturation influences the expression of hormonal effects. In addition, PTH has been shown to both inhibit and accelerate chondrocyte differentiation. Although cyclic AMP (cAMP) is considered the primary mediator of PTH-induced effects on various target cells, the precise role of cAMP-mediated stimulation in chondrocytes is not clear. Numerous studies demonstrating transient increases in cellular cAMP levels shortly after exposing chondrocytes to PTH suggest a mediatory role for this secondary messenger. Additional evidence is provided by the ability of cAMP analogs such as N sub e-monobutyryl cAMP and N sub e, O 2'-dibutyryl-aadenosine 3',5'-cyclic-monophosphate to mimic certain effects of PTH when incubated with chondrocytes in vitro. Nevertheless, recent evidence suggest cAMP s not the only mediator coupling PTH to cellular responses in chondrocytes.