Abstract
Pro-opiomelanocortin (POMC) is a polypeptide precursor known to yield biologically active peptides related to a range of functions. These active peptides include the adrenocorticotropic hormone (ACTH), which is essential for maintenance of adrenal growth and steroidogenesis, and the alpha-melanocyte stimulation hormone, which plays a key role in energy homeostasis. However, the role of the highly conserved N-terminal region of POMC peptide fragments has begun to be unraveled only recently. Here, we review the cascade of events involved in regulation of proliferation and growth of murine adrenal cortex triggered by ACTH and other POMC-derived peptides. Key findings regarding signaling pathways and modulation of genes and proteins required for the regulation of adrenal growth are summarized. We have outlined the known mechanisms as well as future challenges for research on the regulation of adrenal proliferation and growth triggered by these peptides.
Highlights
The primary function of the adrenal cortex is to produce steroids
It has been proposed that adrenocorticotropic hormone (ACTH) induces SAPK/ JNK signaling activation and ERK/MAPK inhibition in vivo [23], results of chronic ACTH treatment in Dex-treated rats showed that ACTH is able to induce a sustained and progressive increase in ERK activation and proliferating cell nuclear antigen (PCNA) expression in all adrenal zones [38]
Asp is capable of cleaving small basic substrates, generating N-terminal peptides of pro-opiomelanocortin (N-POMC) 1–49. These findings suggest the existence of an endogenous mitogenic N-POMC peptide, but no consensus about its identity has been reached
Summary
The primary function of the adrenal cortex is to produce steroids. Each zone of the adrenal cortex synthesizes different steroids in response to endocrine and paracrine stimuli. When adrenal growth occurs to compensate for unilateral adrenalectomy in hypophysectomized rats, neither a decrease in circulating corticosterone nor elevated ACTH levels are observed [16], suggesting the action of neural mediation or other POMC-derived peptides. The concept of tissue-specific cleavage of POMC is acceptable, at least in the adrenal gland, where a serine-protease has been cloned and is responsible for cleaving the pro-gamma-MSH into a 52-residue
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