PLATELET-MEMBRANE FATTY ACIDS, PLATELET AGGREGATION, AND THROMBOXANE FORMATION DURING A MACKEREL DIET

Abstract Oestrogen replacement therapy has been shown to protect postmenopausal women from ischaemic heart disease, strokes and hypertension. The mechanism of protection conferred by oestrogen, although partly attributable to changes in serum lipoproteins, is not fully understood. The present study was undertaken to assess the effect of hormone replacement therapy on the composition of platelet membrane fatty acids in postmenopausal women. These were analysed by gas-liquid chromatography before and six weeks after continuous conjugated equine oestrogen therapy (0·625 mg daily) combined with cyclical therapy with 75 μg l-norgestrel from day 17 to 28 of a 28-day cycle. Each subject acted as her own control. The principal findings of the study were that, following treatment, there was a 16·2% reduction in platelet membrane polyunsaturated fatty acids (P<0·001), an increase of 9·1 and 7·1% in saturated fatty acids and monounsaturated fatty acids respectively (P<0·001) and a 17·8% reduction in arachidonic acid (P<0·003). There was no correlation between changes in membrane fatty acids and serum lipoproteins. This suggests that the changes in membrane composition noted in this study may be a primary effect of hormone replacement therapy, especially oestrogen. Journal of Endocrinology (1996) 148, 207–212

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Platelet Membrane Fatty Acids after Myocardial Infarction: The Effect of Timolol

Clinical Science ◽

10.1042/cs066029p ◽

1984 ◽

Vol 66 (6) ◽

pp. 29P.1-29P

Author(s):

C.G.H. Maidment ◽

S.P. Jones ◽

E.J.A. Lea

Keyword(s):

Myocardial Infarction ◽

Fatty Acids ◽

Platelet Membrane ◽

Membrane Fatty Acids

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Red blood cells and platelet membrane fatty acids in non-dialyzed and dialyzed uremies

Clinica Chimica Acta ◽

10.1016/0009-8981(92)90191-r ◽

1992 ◽

Vol 211 (3) ◽

pp. 155-166 ◽

Cited By ~ 17

Author(s):

Domenico Girelli ◽

Margherita Azzini ◽

Oliviero Olivieri ◽

Patrizia Guarini ◽

Maria Teresa Trevisan ◽

...

Keyword(s):

Fatty Acids ◽

Red Blood Cells ◽

Blood Cells ◽

Platelet Membrane ◽

Membrane Fatty Acids

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Glycoprotein Ib Has a Partial Role in Platelet-von Willebrand Factor Collagen Interaction

Thrombosis and Haemostasis ◽

10.1055/s-0038-1647026 ◽

1988 ◽

Vol 60 (02) ◽

pp. 182-187 ◽

Cited By ~ 2

Author(s):

Morio Aihara ◽

Ken Tamura ◽

Ryuko Kawarada ◽

Keizou Okawa ◽

Yutaka Yoshida

Keyword(s):

Platelet Aggregation ◽

Von Willebrand Factor ◽

Ricinus Communis ◽

Protein S ◽

Platelet Membrane ◽

Membrane Glycoprotein ◽

Normal Plasma ◽

Ricinus Communis Agglutinin ◽

Von Willebrand ◽

Willebrand Factor

SummaryThe adhesion of human fixed washed platelets (FWP) to collagen was decreased after treatment with Serratia marcescens protease (SP), which removed 95% of the glycocalicin from platelet membrane glycoprotein (GP) lb. However, the diminished adhesion of SP treated FWP to collagen could still be increased in the presence of purified von Willebrand factor (vWF). This ability of vWF to increase FWP adhesion to collagen is defined as collagen cofactor (CCo). The adhesion of FWP to collagen was not affected by a monoclonal antibody (MAb) to GP Ilb/IIIa (10E5), that inhibits ADP and collagen induced platelet aggregation. On the other hand, it was decreased by 50% by a MAb to GP lb (6D1), that inhibits ristocetin induced platelet aggregation. Adhesion of FWP in buffer to collagen was completely inhibited by Ricinus communis agglutinin I or concanavalin A, while Lens culinalis agglutinin and wheat germ agglutinin showed 50% inhibition. The FWP adhesion to collagen in the presence of vWF (normal plasma) was unaffected by MAbs to GP Ilb/IIIa (10E5, P2, HPL1) but was decreased to 32-38% by MAbs to GP lb (6D1, AN51, HPL11). A MAb to vWF (CLB-RAg 35), that inhibits ristocetin induced binding of vWF to platelets, decreased the CCo of normal plasma by 70%. The MAb, CLB-RAg 201, that inhibits the binding of vWF to collagen, completely inhibited the CCo of normal plasma. In conclusion, our data suggest that (1) GP lb has a partial role in FWP adhesion to collagen; (2) the binding of vWF to collagen is required for the expression of CCo; (3) CCo is partly mediated through GP lb; but (4) other platelet membrane protein(s) besides GP lb or GP Ilb/IIIa must also be involved in FWP-vWF-collagen interactions.

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Trimucytin: A Collagen-Like Aggregating Inducer Isolated from Trimeresurus mucrosquamatus Snake Venom

Thrombosis and Haemostasis ◽

10.1055/s-0038-1651597 ◽

1993 ◽

Vol 69 (03) ◽

pp. 286-292 ◽

Cited By ~ 13

Author(s):

Che-Ming Teng ◽

Feng-Nien Ko ◽

Inn-Ho Tsai ◽

Man-Ling Hung ◽

Tur-Fu Huang

Keyword(s):

Platelet Aggregation ◽

Snake Venom ◽

Inositol Phosphate ◽

Shape Change ◽

Platelet Activating Factor ◽

Atp Release ◽

Platelet Membrane ◽

Thromboxane B2 ◽

Dependent Manner ◽

Concentration Dependent Manner

SummaryTrimucytin is a potent platelet aggregation inducer isolated from Trimeresurus mucrosquamatus snake venom. Similar to collagen, trimucytin has a run of (Gly-Pro-X) repeats at the N-terminal amino acids sequence. It induced platelet aggregation, ATP release and thromboxane formation in rabbit platelets in a concentration-dependent manner. The aggregation was not due to released ADP since it was not suppressed by creatine phosphate/creatine phosphokinase. It was not either due to thromboxane A2 formation because indomethacin and BW755C did not have any effect on the aggregation even thromboxane B2 formation was completely abolished by indomethacin. Platelet-activating factor (PAF) was not involved in the aggregation since a PAF antagonist, kadsurenone, did not affect. However, RGD-containing peptide triflavin inhibited the aggregation, but not the release of ATP, of platelets induced by trimucytin. Indomethacin, mepacrine, prostaglandin E1 and tetracaine inhibited the thromboxane B2 formation of platelets caused by collagen and trimucytin. Forskolin and sodium nitroprusside inhibited both platelet aggregation and ATP release, but not the shape change induced by trimucytin. In quin-2 loaded platelets, the rise of intracellular calcium concentration caused by trimucytin was decreased by 12-O-tetradecanoyl phorbol-13 acetate, imipramine, TMB-8 and indomethacin. In the absence of extracellular calcium, both collagen and trimucytin caused no thromboxane B2 formation, but still induced ATP release which was completely blocked by R 59022. Inositol phosphate formation in platelets was markedly enhanced by trimucytin and collagen. MAB1988, an antibody against platelet membrane glycoprotein Ia, inhibited trimucytinand collagen-induced platelet aggregation and ATP release. However, trimucytin did not replace the binding of 125I-labeled MAB1988 to platelets. Platelets pre-exposed to trimucytin were resistant to the second challenge with trimucytin itself or collagen. It is concluded that trimucytin may activate collagen receptors on platelet membrane, and cause aggregation and release mainly through phospholipase C-phosphoinositide pathway.

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Platelet Aggregation in Finnish Men and Its Relation to Fatty Acids in Platelets, Plasma and Adipose Tissue

Thrombosis and Haemostasis ◽

10.1055/s-0038-1660071 ◽

1985 ◽

Vol 54 (03) ◽

pp. 563-569 ◽

Cited By ~ 19

Author(s):

M K Salo ◽

E Vartiainen ◽

P Puska ◽

T Nikkari

Keyword(s):

Fatty Acids ◽

Adipose Tissue ◽

Fatty Acid Composition ◽

Fatty Acid ◽

Platelet Aggregation ◽

Acid Composition ◽

Saturated Fatty Acids ◽

Free Living ◽

Ω3 Fatty Acids ◽

Induced Aggregation

SummaryPlatelet aggregation and its relation to fatty acid composition of platelets, plasma and adipose tissue was determined in 196 randomly selected, free-living, 40-49-year-old men in two regions of Finland (east and southwest) with a nearly twofold difference in the IHD rate.There were no significant east-southwest differences in platelet aggregation induced with ADP, thrombin or epinephrine. ADP-induced platelet secondary aggregation showed significant negative associations with all C20-C22 ω3-fatty acids in platelets (r = -0.26 - -0.40) and with the platelet 20: 5ω3/20: 4ω 6 and ω3/ ω6 ratios, but significant positive correlations with the contents of 18:2 in adipose tissue (r = 0.20) and plasma triglycerides (TG) (r = 0.29). Epinephrine-induced aggregation correlated negatively with 20: 5ω 3 in plasma cholesteryl esters (CE) (r = -0.23) and TG (r = -0.29), and positively with the total percentage of saturated fatty acids in platelets (r = 0.33), but had no significant correlations with any of the ω6-fatty acids. Thrombin-induced aggregation correlated negatively with the ω3/6ω ratio in adipose tissue (r = -0.25) and the 20: 3ω6/20: 4ω 6 ratio in plasma CE (r = -0.27) and free fatty acids (FFA) (r = -0.23), and positively with adipose tissue 18:2 (r = 0.23) and 20:4ω6 (r = 0.22) in plasma phospholipids (PL).The percentages of prostanoid precursors in platelet lipids, i. e. 20: 3ω 6, 20: 4ω 6 and 20 :5ω 3, correlated best with the same fatty acids in plasma CE (r = 0.32 - 0.77) and PL (r = 0.28 - 0.74). Platelet 20: 5ω 3 had highly significant negative correlations with the percentage of 18:2 in adipose tissue and all plasma lipid fractions (r = -0.35 - -0.44).These results suggest that, among a free-living population, relatively small changes in the fatty acid composition of plasma and platelets may be reflected in significant differences in platelet aggregation, and that an increase in linoleate-rich vegetable fat in the diet may not affect platelet function favourably unless it is accompanied by an adequate supply of ω3 fatty acids.

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