Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Gries, A; Gries, M; Wurm, H; Kenner, T; Ijsseldijk, M; Sixma, JJ; Kostner, GM.
Lipoprotein(a) inhibits collagen-induced aggregation of thrombocytes.
Arterioscler Thromb Vasc Biol. 1996; 16(5):648-655
Doi: 10.1161/01.ATV.16.5.648
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- Führende Autor*innen der Med Uni Graz
- Gries Anna
- Co-Autor*innen der Med Uni Graz
- Kenner Thomas
- Kostner Gerhard
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- Abstract:
- Lipoprotein(a) [Lp(a)] is known to interact with human platelets in vitro. In the present study the effect of physiological concentrations of Lp(a) on platelet aggregation was studied. Freshly prepared gel-filtered platelets from healthy donors were incubated for 30 minutes at 37 degrees C with various concentrations of Lp(a); aggregation was triggered with ADP, thrombin, and collagen. Control incubations were performed with Tyrode's solution or LDL. Thrombin- and ADP-triggered aggregations were only slightly influenced by Lp(a), but aggregation of platelets stimulated with collagen (4 micrograms/mL) was markedly inhibited. Measurable effects occurred at low concentrations (0.05 mg/mL) of total Lp(a); at 0.5 mg/mL, maximum aggregation of platelets was inhibited by 54 +/- 20%, and the aggregation rate was attenuated by 47 +/- 19% compared with platelets incubated with Tyrode's solution. Preincubation of collagen (4 micrograms/mL) with Lp(a) yielded similar results. The effect of Lp(a) on platelet aggregation was accompanied by a significant reduction of serotonin release and TXA2 formation. Higher concentrations of collagen ( > or = 10 micrograms/ mL) caused the inhibitory effect on Lp(a) on collagen-induced aggregation to disappear. In contrast, incubation of platelets with 5 mg/mL LDL led to a significant increase of aggregation rate, maximum aggregation, serotonin release, and formation of TXA2 when aggregation was induced with 4 micrograms/mL collagen. In an adhesion assay using fresh whole blood, which mimics the in vitro situation of vessel injury. Lp(a) reduced platelet adhesion at shear rates of 300 and 1600/s by 22.6% and 11.6%, respectively. In addition, Lp(a) reduced the size of platelet aggregates significantly (up to 63%); this reduction was more distant at the higher shear rate. Unlike LDL, Lp(a) is not a proaggregatory lipoprotein; rather, collagen-triggered aggregation in vitro is attenuated by Lp(a).
- Find related publications in this database (using NLM MeSH Indexing)
- Blood Platelets - metabolism
- Collagen - pharmacology
- Female - pharmacology
- Humans - pharmacology
- Lipoprotein(a) - pharmacology
- Male - pharmacology
- Perfusion - pharmacology
- Platelet Adhesiveness - drug effects
- Serotonin - metabolism
- Thromboxane B2 - biosynthesis
- Find related publications in this database (Keywords)
- Lipoprotein(A)
- Platelet Aggregation
- Serotonin Release
- Thromboxane A(2)
- Platelet Adhesion