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Mattos GE. Signaling pathways and biological effects of corticotropin (ACTH), proopiomelanocortin NH2-terminal peptide (N-POMC) and fibroblast growth factor type 2 (FGF2) in rat adrenal primary culture cells. [Ph. D. thesis (Morphofunctional)]. São Paulo: Instituto de Ciências Biomédicas, Universidade de São Paulo; 2011. Cell proliferation is a complex process, primarily regulated by external growth factors. One of the main factors that regulate adrenal cortex is the adrenocorticotrophic hormone (ACTH), however there are evidences that other peptide factors such as the fibroblast growth factor type 2 (FGF2) and pro-opiomelanocortin N-terminal fragments (N-POMC) might also be involved. The mitogen-activated protein kinase (MAPK) pathways, ERK, JNK and p38, together with other signaling pathways such as PKA, PKC and PI3K/Akt integrate signals from a diverse range of stimuli and trigger responses as proliferation, differentiation, survival and cell death. Although there are great advances regarding ACTH and FGF2 action in human and mice tumor cell lines, this action is still little known in normal adrenocortical cells, especially regarding N-POMC peptides effects. In the present study we analyze the importance of these pathways and their influence in biological responses such as viability, cell proliferation and cell death stimulated by ACTH, FGF2 and N-POMC peptides, with N-POMC and without N-POMC disulfide bridges, using specific pharmacological and molecular inhibitors in a well-characterized isolated primary culture of Glomerulosa (G) and Fasciculata/Reticularis cells (F/R). Our results show that FGF2 and N-POMC peptides trigger cell proliferation while ACTH stimulates progressive loss of metabolic activity and viability, dicrease proliferation and cell death by apoptosis. Through the analysis of pharmacological and molecular inhibitors it was shown that the mediating signaling pathways involved in FGF2 and N-POMC proliferative effects are, respectively, ERK/JNK and ERK/JNK/Akt. On the other hand, the pro-apoptotic response promoted by ACTH is through p38 signaling, probably associated with the absence of activation of other pathways involved with cell survival, like ERK and JNK.

Vias de sinalização e efeito biológico da corticotropina (ACTH), do peptídeo NH2-terminal da pró-opiomelanocortina (N-POMC) e do fator de crescimento de fibroblastos (FGF2) em culturas primárias de células da suprarrenal de rato.