EFFECT OF DEHYDROEPIANDROSTERONE ON THE SECRETION OF PROSTAGLANDIN I_2 IN HUMAN AORTIC SMOOTH MUSCLE CELLS

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Prostaglandin I_2 (PGI_2) is a vasodilatory prostaglandin that is considered to be anti-atherogenic. There have been many reports regarding the relationship between the serum level of dehydroepiandrosterone (DHEA) and atherosclerotic disease. We have previously demonstrated that DHEA inhibits mitogen-activated protein kinase (MAPK) activation via overproduction of prostaglandin (PG) in human male aortic smooth muscle cells (HASMC). The objective of the present study was to determine whether DHEA modifies the secretion of PGI_2. We showed that DHEA stimulates the release of PGI_2 (1.5-to 3-fold compared to the control) over an incubation period of 4 to 8h. This stimulatory effect of DHEA was not affected by an aromatase inhibitor and was partially blocked by a protein kinase C inhibitor. Immunoblot analysis showed that DHEA treatment enhanced the protein expression of cytosolic phosphokipase A_2 (cPLA_2) but did not alter the protein expression of cyclooxygenase (COX)-1 or COX-2 compared to control cells. The effect of DHEA on cPLA_2 production in HASMC was opposite to that previously reported for glucocorticoids, such as dexamethasone in several cell types. We concluded that DHEA stimulated prostacyclin secretion via an increase in cPLA_2 production in HASMC.
2010-09-01

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