Abstract
The N-terminal fragment of pro-opiomelancortin (POMC) has been shown previously to act as an adrenal mitogen. However, little is known about the molecular mechanisms by which mitogenesis is stimulated, although it has been shown that N-POMC1–28 stimulates the ERK pathway in human H295R cells. We have investigated signaling stimulated by N-POMC1–28 and N-POMC1–49 in the mouse Y1 cell line and found that both peptides stimulate ERK phosphorylation with maximal stimulation being achieved within 5 min. Similar results were observed for both MEK and c-Raf phosphorylation, although N-POMC1–49 stimulated the phosphorylation of Akt more robustly than N-POMC1–28.We also investigated the expression of tyrosine kinase receptors in adrenal cells. PCR utilizing degenerate primers was performed on cDNA from both Y1 cells and rat adrenal tissue. Sequencing of 114 clones from each cDNA population revealed the expression of a number of receptors, several of which have not been described previously in the adrenal.
Highlights
The cortex of the mammalian adrenal gland is subdivided into three concentric zones that are both functionally and morphologically distinct
Since synthetic N-POMC1-28 has been shown previously to activate p44/42 ERK (Fassnacht et al, 2003) we were interested to see if this peptide could activate this signaling pathway in the commonly used mouse Y1 adrenocortical cell line
We were interested to investigate if the longer N-POMC1-49 peptide could activate this pathway and in a similar manner to N-POMC1-28
Summary
The cortex of the mammalian adrenal gland is subdivided into three concentric zones that are both functionally and morphologically distinct. It is believed that all the cells in the cortex are derived from a narrow band of stem cells located at the periphery of the gland and the daughter cells migrate towards the centre of the gland phenotypically switching into the various functional zones before undergoing apoptosis at the zona reticularis/medulla boundary (Estivariz et al, 1992) This proliferation is dependent upon peptides derived from the ACTH precursor pro-opiomelanocortin (POMC) since surgical removal of the pituitary (Deane and Greep, 1946) or suppression of corticotroph activity using dexamethasone (Bransome, 1968; Wright et al, 1974) (which results in down regulation of all POMC peptides) results in adrenal atrophy. It aimed to survey the expression of receptor tyrosine kinase molecules in an attempt to identify a possible candidate by which N-POMC could stimulate adrenal cell proliferation
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