Increased extracellular signal regulated kinases phosphorylation in the adrenal gland in response to chronic ACTH treatment.

摘要: ACTH released from the pituitary acts through activation of cAMP/PKA in adrenocortical cells stimulating steroidogenesis. Although was originally thought to have anti-proliferative effects on adrenal, recently it has been described that could also proliferative acting other signalling cascades. This is relevant humans given increased levels occurring together with adrenal cortex hyperplasia observed Cushing's disease and possibly situations such as chronic stress. One pathways regulating cell proliferation extracellular signal regulated kinase (ERKs) pathway. ERKs are members MAPK family They activated by stimuli growth factors mitogens, become phosphorylated MEK1/2 regulate a diversity cellular processes differentiation. Until now, no study addressed administration vivo. Using rats submitted different dosages well variable durations, we determined if induced establishing parallelism proliferating nuclear antigen (PCNA) expression, aimed demonstrate role ACTH-induced proliferation. Blood collected for hormonal analysis stimulation steroidogenesis studied. We confirmed weight corticosterone when compared control or dexamethasone-treated animals. demonstrated increases PCNA expression time- dose-dependent manner. When blocked use specific MEK inhibitor (PD98059), there decrease release expression. conclude induces this plays an important induction