p44/42(ERK1/2) MAPK and PLD activation by PGD2 preserves papillary phosphatidylcholine homeostasis.

Previous works from our laboratory demonstrated that PGD(2) modulates phosphatidylcholine (PC) biosynthesis in renal papillary tissue. In the present work, we have evaluated the mechanism by which PGD(2) exerts this action. PGD(2) caused two stimulatory waves in PC synthesis which were reproduced by its full-agonist BW245C.

COX-2-mediated PGD2 synthesis regulates phosphatidylcholine biosynthesis in rat renal papillary tissue.

Phosphatidylcholine (PC) is the major membrane phospholipid in mammalian cells. Previous works from our laboratory demonstrated a close metabolic relationship between the maintenance of PC biosynthesis and the prostaglandins endogenously synthesized by cyclooxygenase (COX) in rat renal papilla. In the present work, we studied the COX isoform involved in papillary PC biosynthesis regulation.

Phospholipase C inhibitors and prostaglandins differentially regulate phosphatidylcholine synthesis in rat renal papilla. Evidence of compartmental regulation of CTP:phosphocholine cytidylyltransferase and CDP-choline:1,2-diacylglycerol cholinephosphotransferase.

Phosphatidylcholine (PC) is the most abundant phospholipid in mammalian cell membranes. Several lines of evidence support that PC homeostasis is preserved by the equilibrium between PC biosynthetic enzymes and phospholipases catabolic activities. We have previously shown that papillary synthesis of PC depends on prostaglandins (PGs) that modulate biosynthetic enzymes.

Enhancement of phosphatidylcholine biosynthesis by angiotensin-(1-7) in the rat renal cortex.

In the present paper, we investigated the effect of angiotensin-(1-7) (Ang-(1-7)) on phospholipid biosynthesis in the rat renal cortex. A significant increase in phosphatidylcholine (PC) labeling was observed when cortical slices, prelabeled with [32P]orthophosphate, were incubated for 30 min in the presence of Ang-(1-7) (1 pM to 100 nM). Neither the phospholipase C inhibitors, neomycin or db-cAMP nor the protein kinase C inhibitors, chelerythrine or H7, modified the stimulatory effect induced by 0.