Effect of PGE 2 on the cell surface molecule expression in PMA treated thymocytes

Abstract

PGE 2 is produced by cells of the thymic microenvironment. The effects of PGE 2 are mediated by cAMP through binding to its intracellular receptor protein kinase A (PKA). Phorbol 12-myristate 13-acetate (PMA) is known to modulate CD molecule expression on thymocytes, probably through activation of protein kinase C (PKC). We have hypothesized that cross-talk between these two signalling pathways may affect modulation of the CD molecules on the cell surface of thymocytes. For this purpose, we compare the effects of PMA alone or combined with PGE 2 on CD3, CD4 and CD8 expression on mouse thymocytes by flow-cytometric analysis. PMA treatment almost completely abolished CD4 expression and slightly decreased CD3 and CD8 expression. PGE 2 alone did not change the CD3, CD4 and CD8 molecule expression. Combined with PMA, PGE 2 can overcome the decrease induced by PMA of the CD3 expression and partially reduced the disappearance of the CD4 molecule. On the other hand PGE 2 accelerated the loss of CD8 molecule expression. These events occurred only in CD4+ CD8+ immature thymocytes. An analogue of cAMP (dibutryl cAMP) mimics the effect of PGE 2, but not Br-cGMP. This differential regulation by PGE 2 of the CD molecule expression on immature thymocytes may provide additional evidence on the role of PGE 2 during the process of thymic differentiation.