Mobilization of arachidonic acid in human platelets kinetics and Ca2+ dependency

Rittenhouse-Simmons, S; Russell, Francis A.; Deykin, Daniel

doi:10.1016/0005-2760(77)90196-5

Cited by 139 publications

(37 citation statements)

References 21 publications

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“…The ethanolamine phosphoglycerides have a high content of arachidonate (10)(11)(12) and this was used as evidence favoring PE as a source of free arachidonate by these investigators (30). In contrast, Rittenhouse-Simmons et al (31), using a different approach, suggested the plasmalogen form of PE as a source of arachidonate for cyclooxygenase and lipoxygenase. Partial purification of platelet phospholipase A2 has been described (32)(33)(34)(35).…”

Section: Resultsmentioning

confidence: 99%

Phospholipid Metabolism in Stimulated Human Platelets

Broekman¹,

Ward²,

Marcus³

1980

J. Clin. Invest.

344

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Section: Resultsmentioning

confidence: 99%

Phospholipid Metabolism in Stimulated Human Platelets

Broekman¹,

Ward²,

Marcus³

1980

J. Clin. Invest.

344

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“…For studies on the metabolismn of radiolabeled arachi(loniic acid or glycerol, PRP was incuibated with [5,6,8,9,11,12,14,15-3H]arachidonic acid (12.5 ,uCi/30 ml PRP, 72 Ci/mmol) which had been hound to albuumin as described previously (14) (8,19). Radioactivity contained in the lipid spots wvas counted by scintillationi spectrophotometry in H20-AqIuasol (New England Nuclear) (8), and lipid phosphorus was assayed after dligestioni of parallel samiiples (19). Neutral lipids were resolved by thin-laver chromatography in solvent systems I and II.…”

Section: Methodsmentioning

confidence: 99%

“…Therefore, those chaniges in lipid metabolism that may participate in promoting secretioni must be well underway within this period. The rapid generation of cyclic endoperoxides derived from arachidonic acid released frolm PI and phosphatidylcholine (PC) is one such change (7)(8)(9)(10). Additional short-term effects characterized thus far in platelets exposed to agents such as collagen, ADP, and thrombin have been an increased incorporation of [32P]orthophosphate into phosphatidic acid and polyphosphoinositides (11) and a decrease in the amount of previously radiolabeled PI (12).…”

Section: Introductionmentioning

confidence: 99%

Production of diglyceride from phosphatidylinositol in activated human platelets.

1979

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“…Endogenous arachidonic acid is released from platelet phospholipids when platelets are stimulated with an agent such as thrombin (32,33). As much as 20 nmol per 109 platelets is released by maximal stimulation (32).…”

Section: Discussionmentioning

confidence: 99%

“…The platelet dense granule pool was labeled with ['4C]serotonin, and labeled gelfiltered platelets (GFP) were prepared as described (3). The procedure yielded [30][31][32][33][34][35][36][37][38][39][40] ml of labeled GFP containing 1-3 X 108 platelets per ml.…”

mentioning

confidence: 99%

Release of platelet-derived growth factor from human platelets by arachidonic acid

Linder

Chernoff

Kaplan

et al. 1979

Proc. Natl. Acad. Sci. U.S.A.

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Platelet a-granules contain a factor that stimulates the proliferation of arterial smooth muscle cells and may play a role in atherogenesis. We have studied the role of arachidonic acid in mediating the release of the platelet-derived growth factor (PDGF) from human platelets. PDGF was assayed by stimulation of [3Hlthymidine incororation into DNA of mouse 3T3 cells. Platelet aggregation and the release of platelet factor 4, P-thromboglobulin, and serotonin were also studied.A biphasic response pattern was observed when gel-filtered platelets were incubated with arachidonate over the concentration range 0.01-0.4 mM. At low arachidonate levels (approximately 0.025-0.1 mM), specific concentration-dependent aggregation and release of PDGF and of the other components were observed. This effect was not seen with any of five other fatty acids tested and was suppressed by indomethacin (25 uM). At higher arachidonate concentrations (approximately 0.15-0.35 mM), a concentration-dependent turn-off of both aggregation and release occurred. At these concentrations the platelets remained functional, and no release of lactate dehydrogenase was observed. A similar biphasic pattern of arachidonate-induced aggregation and release was observed with platelet-rich plasma, over a similar range of arachidonate to albumin mole ratios. These studies demonstrate that PDGF and other a-granule constituents can be released from platelets specifically by arachidonate via an indomethacin-sensitive pathway, most probably involving the platelet cyclooxygenase and conversion of arachidonate to prostaglandin metabolites. The mechanisms responsible for the turn-off of the specific arachidonate-mediated responses at higher arachidonate concentrations remain to be defined.

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Mobilization of arachidonic acid in human platelets kinetics and Ca2+ dependency

Cited by 139 publications

References 21 publications

Phospholipid Metabolism in Stimulated Human Platelets

Phospholipid Metabolism in Stimulated Human Platelets

Production of diglyceride from phosphatidylinositol in activated human platelets.

Release of platelet-derived growth factor from human platelets by arachidonic acid

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