Modulation of rat brain cytosolic phosphatidate phosphohydrolase: Effect of cationic amphiphilic drugs and divalent cations

Koul, Omanand; Hauser, George

doi:10.1016/0003-9861(87)90199-8

Cited by 96 publications

(41 citation statements)

References 36 publications

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“…To more carefully assess the action of the direct formation of DG by PC-PLC, the other DG pathway by PLD was examined. Propranolol, commonly used as an inhibitor of PA phosphohydrolase [20], did not affect DG production in response to HGF. Furthermore, in the presence of ethanol, PLD catalyzes the transphosphatidylation of PC to yield a specific phospholipid, phosphatidylethanol (PEt) which is a useful marker for PLD activity [21].…”

Section: Resultsmentioning

confidence: 79%

Hepatocyte growth factor (HGF) mediates the sustained formation of 1,2‐diacylglycerol via phosphatidylcholine—phospholipase C in cultured rat hepatocytes

et al. 1992

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The addition of hepatocyte growth factor (HGF) to rat hepatocytes in primary culture resulted in the formation of inositol 1,4,5‐trisphosphate (Ins(1,4,5)P3) and 1,2‐diacylglycerol (DG) by a phosphoinositide‐specific phospholipase C (PI‐PLC). DG showed a biphasic increase; the first phase, corresponding with the peak of Ins(1,4,5)P3 and a second larger and prolonged phase. The HGF stimulates the phosphatidylcholine (PC)‐derived prolonged DG formation by a phospholipase C pathway (PC‐PLC) but not by a phospholipase D pathway. HGF also was found to elicit [Ca2+] oscillations which may be associated with the prolonged DG production from PC via the PC‐PLC phospholipase C pathway.

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Section: Resultsmentioning

confidence: 79%

Hepatocyte growth factor (HGF) mediates the sustained formation of 1,2‐diacylglycerol via phosphatidylcholine—phospholipase C in cultured rat hepatocytes

et al. 1992

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“…The addition of unlabeled myristic acid (9/~M), either during the 60 min chase (postlabeling) or at the time of TPA addition, had no influence on the formation of [3H]PA or [3H]DG. The kinetics for the formation of [~H]myristoyl-DG indicate that the DG is derived from PA. To verify this point, cells were preincubated with propranolol, a phosphatidate phosphohydrolase inhibitor [14]. Preliminary experiments showed that 100/zM propranolol was sufficient to block TPAinduced DG formation.…”

Section: Resultsmentioning

confidence: 99%

The phosphatidylcholine pathway of diacylglycerol formation stimulated by phorbol diesters occurs via phospholipase D activation

et al. 1988

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Agonist-induced degradation of phosphatidylcholine (PC) is of interest as this pathway of diacylglycerol (DG) generation may provide added opportunities for the regulation of protein kinase C (PKC). In REF52 cells pH]myristic acid is preferentially incorporated into PC; this, coupled with the use of pH]eholine, allows for quantitation of both the water-soluble and the lipid products generated when PC is degraded. In cells prelabeled with pH]choline, TPA stimulated a time-dependent release, into the medium, of choline and not phosphocholine or glycerophosphocholine. Treatment of pH]myristic acid-labeled cells with either phorbol diesters, sn-1,2-dioetanoyiglycerol, or vasopressin elicited the formation of labeled phosphatidate (PA) and DG. The temporal pattern of PC hydrolysis in cells treated with TPA is indicative of a precursor (PA)-product (DG) relationship for an enzymatic sequence initiated by phospholipase D. Adding propranolol, a phosphatidate phosphohydrolase inhibitor, eliminated TPA-induced DG formation, whereas PA generation was unaffected. From these data we conclude that TPA elicits DG formation from PC by the sequential actions of phospholipase D and phosphatidate phosphohydrolase.

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“…Incubation of neutrophils with [3H]palmitic acid resulted in selective radioactive labelling of PtdCho, and 3H-labelled PtdEtOH accumulated in cells incubated with either fMLF or TPA in the presence of ethanol. Conversely, fatty acids did not stimulate the accumulation of 3H-labelled PtdEtOH, indicating that the respiratory burst induced by these agents is independent of the hydrolysis of PtdCho by phospholipase D. Consequently, the inhibition of the fattyacid-induced respiratory burst by ethanol and propranolol, agents known to interfere with the cascade initiated by phospholipase D in a number of systems, including neutrophils (Dawson, 1967;Koul and Hauser, 1987;Billah et al, 1989b;Mullmann et al, 1990;Rossi et al, 1990), was unexpected. It is of course possible that these compounds influence the respiratory burst by mechanisms unrelated to phospholipase D. Alternatively, neutrophils may contain a fatty-acid-activated phospholipase D with specificity towards phospholipids other than PtdCho, or the fatty acids may interact with the cell membrane and alter the presentation of phospholipid species to phospholipase D. There is evidence that neutrophils have the capacity to hydrolyse phospholipids other than PtdCho via phospholipase D, although the situation is far from clear.…”

Section: Discussionmentioning

confidence: 99%

The neutrophil respiratory burst

Hardy

Robinson

Poulos

et al. 1991

European Journal of Biochemistry

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The oxygen-dependent respiratory burst is a key neutrophil function required for the killing of bacteria. However, despite intensive investigation, the molecular events which initiate the respiratory burst remain unclear. Recent reports have suggested the agonist-induced hydrolysis of cellular phosphatidylcholine (PtdCho) by phospholipase D may be an essential requirement for initiating or mediating the respiratory burst. We have investigated the effects of the chemotactic peptide N-formylmethionylleucylphenylalanine (fMLF), the phorbol ester 12-0-tetradecanoyl-phorbol 13-acetate (TPA) and the polyunsaturated fatty acids arachidonic [20 : 4 (n-6)] and docosahexaenoic [22 : 6 (n-3)] acids in light of this hypothesis. Ethanol-inhibited superoxide production in response to 20:4, 22:6 and fMLF, in a dose-dependent fashion, suggesting an involvement of phospholipase D. The phosphatidic-acid phosphohydrolase inhibitor DL-propranolol completely inhibited superoxide production induced by both 20:4 and 22:6, and partially inhibited the response to TPA. In contrast, superoxide production in response to fMLF was increased by propranolol. fMLF and TPA, but not the fatty acids, stimulated phospholipase D as indicated by the accumulation of phosphatidic acid and, in the presence of ethanol, phosphatidylethanol derived from PtdCho. Extracellular Ca2+ was found to be an essential requirement for fMLF-induced superoxide production. However, responses to the fatty acids were dramatically enhanced under Ca2',-free conditions. Responses to TPA were independent of the extracellular Ca2+ concentration. Both fatty acids and fMLF, but not TPA, mobilised Ca2+ from intracellular stores, a response insensitive to the effects of both ethanol and propranolol. These results show that, unlike fMLF and TPA, the fatty acids do not cause hydrolysis of PtdCho by phospholipase D. However, the data indirectly suggests that the fatty acids may initiate the phospholipase-D-catalysed hydrolysis of phospholipids other than PtdCho.The oxygen-dependent respiratory burst is a major biochemical response in neutrophils that is associated with their interaction with various types of soluble and particulate stimuli. This response is mediated by a membrane-bound flavoproteinlb-type cytochrome complex, the NADPH oxidase, which catalyses the reduction of molecular oxygen to superoxide (reviewed by Rossi, 1986; Bdbior, 1988;Segel, 1989). However, the sequence of events following ligand interaction with the cell surface which ultimately lead to oxyradical production are not well understood. Receptor binding has been shown to initiate the hydrolysis of inositol phosphates, resulting in the production of the intracellular messengers, inositol 1,4,5-trisphosphate and diacylglycerol (reviewed by Cockcroft, 1989). Inositol 1,4,5-trisphosphate has been reported to mobilise Ca2+ from intracellular stores, whileCorrespondence to A.

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Modulation of rat brain cytosolic phosphatidate phosphohydrolase: Effect of cationic amphiphilic drugs and divalent cations

Cited by 96 publications

References 36 publications

Hepatocyte growth factor (HGF) mediates the sustained formation of 1,2‐diacylglycerol via phosphatidylcholine—phospholipase C in cultured rat hepatocytes

Hepatocyte growth factor (HGF) mediates the sustained formation of 1,2‐diacylglycerol via phosphatidylcholine—phospholipase C in cultured rat hepatocytes

The phosphatidylcholine pathway of diacylglycerol formation stimulated by phorbol diesters occurs via phospholipase D activation

The neutrophil respiratory burst

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