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Sun Kyu Park

Publications and source records attributed to Sun Kyu Park.

2 recordsLinked to original sources

The expression patterns of RGS transcripts in platelets.

Regulators of G protein signalling (RGS) are involved in the negative regulation of cell activation processes and are involved in the pathophysiology of cardiovascular diseases. To get some further evidence for a role of RGS proteins in platelets, we determined the expression profile of RGS-specific mRNA in rat platelets using reverse transcription-polymerase chain reaction (RT-PCR) with a poly dT18 primer and transcript-specific primers. We found that RGS2, RGS3, RGS5, RGS6, RGS10, RGS14, RGS16 and RGS18, Leukemia-associated Rho-GEF factor (LARG), and Galpha interacting protein (GAIP) were differentially expressed in platelets. The highest expression rate was found for RGS18 (about 1.3 fold when compared to GAPDH), followed by LARG, RGS6, RGS10 and RGS16 (0.7 to 0.95), whereas expression rates for RGS2, RGS3, RGS5, RGS14, and GAIP were in a range of 0.1 to 0.3. Our results suggest that G-protein-coupled receptor-mediated signalling in platelet may be regulated mainly by RGS 18, 16, 10, 6, and LARG.

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Surfactin C inhibits platelet aggregation.

This study was designed to investigate the effect of surfactin C, which is derived from Bacillus subtilis, on platelet aggregation and homotypic leucocyte aggregation. Surfactin C strongly and dose-dependently inhibited platelet aggregation, which was stimulated both by thrombin (0.1 U mL(-1)), a potent agonist that activates the G protein-coupled protease receptor, and by collagen (5 microg mL(-1)), a potent ligand that activates alpha(IIb)beta(3) with IC50 values (concentration inhibiting platelet aggregation by 50%) of 10.9 and 17.0 microM, respectively. Moreover, surfactin C significantly suppressed the intracellular Ca(2+) mobilization in thrombin-activated platelets. Surfactin C, however, did not affect various integrin-mediated U937 cell aggregation, implying that the anti-platelet activity of surfactin C was not due to its detergent effect but by its action on the downstream signalling pathway. Therefore, the results suggest that surfactin C may have a beneficial therapeutic effect on aberrant platelet aggregation-mediated cardiovascular diseases.

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