Effect of P2Y1 and P2Y12 genetic polymorphisms on the ADP-induced platelet aggregation in a Korean population

Kyoung Ah Kim, Wan Geun Song, Hye Mi Lee, Hyun Jin Joo, Ji-Young Park

Research output: Contribution to journalArticle

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Abstract

Background P2Y1 and P2Y12 receptors are expressed in platelet membranes and are involved in ADP-induced platelet aggregation. Genetic polymorphisms of P2Y1 and P2Y12 play a major role in the variation of ADP-induced platelet aggregation and in response in antiplatelet therapy. Objective To evaluate the allele frequencies of P2Y1 and P2Y12 genetic polymorphisms in a Korean population and to assess their role in ADP (5 μmol/L)-induced maximal platelet aggregation. Methods P2Y1 (c.1622A > G) and P2Y12 (i-139C > T, i-744 T > C, i-ins801, c.52G > T, c.34C > T) polymorphisms were analyzed in 158 Korean healthy participants using pyrosequencing methods. Their ADP-induced maximal platelet aggregation was assessed by the turbidometric method. Results The observed allele frequencies of P2Y1 and P2Y12 were as follows: 0.3101 for P2Y1 c.1622A > G; 0.1804 for P2Y12 i-139C > T, 0.1804 for i-744 T > C, 0.1804 for i-801insA, 0.1266 for P2Y12 c.52G > T, and 0.2658 for P2Y12 c.34C > T. ADP-induced maximal platelet aggregation was not influenced by the P2Y 1 c.1622A > G polymorphism and was also not affected by three intronic P2Y12 polymorphisms and the P2Y12 c.34C > T polymorphism. However, the P2Y12 c.52G > T polymorphism caused a substantial difference in ADP-induced maximal platelet aggregation (62.75% for c.52GG, 66.27% for c.52GT, and 80.60% for c.52TT; P = 0.0092). Conclusions The P2Y1 and P2Y12 genes were very polymorphic in a Korean population. Three intronic P2Y12 polymorphisms (i-139C > T, i-744 T > C, i-801insA) were in complete linkage disequilibrium but not with the c.52C > T polymorphism in this population. Maximal platelet aggregation in response to ADP is associated with the c.52C > T polymorphism but not with the three intronic polymorphisms or the P2Y1 c.1622A > T polymorphism.

Original languageEnglish
Pages (from-to)221-226
Number of pages6
JournalThrombosis Research
Volume132
Issue number2
DOIs
Publication statusPublished - 2013 Aug 1

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Genetic Polymorphisms
Platelet Aggregation
Adenosine Diphosphate
Population
Gene Frequency
Purinergic P2Y1 Receptors
Linkage Disequilibrium
Healthy Volunteers
Blood Platelets
Membranes
Genes

Keywords

  • ADP
  • P2Y
  • P2Y
  • Platelet aggregation
  • Polymorphism

ASJC Scopus subject areas

  • Hematology

Cite this

Effect of P2Y1 and P2Y12 genetic polymorphisms on the ADP-induced platelet aggregation in a Korean population. / Kim, Kyoung Ah; Song, Wan Geun; Lee, Hye Mi; Joo, Hyun Jin; Park, Ji-Young.

In: Thrombosis Research, Vol. 132, No. 2, 01.08.2013, p. 221-226.

Research output: Contribution to journalArticle

Kim, Kyoung Ah ; Song, Wan Geun ; Lee, Hye Mi ; Joo, Hyun Jin ; Park, Ji-Young. / Effect of P2Y1 and P2Y12 genetic polymorphisms on the ADP-induced platelet aggregation in a Korean population. In: Thrombosis Research. 2013 ; Vol. 132, No. 2. pp. 221-226.
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abstract = "Background P2Y1 and P2Y12 receptors are expressed in platelet membranes and are involved in ADP-induced platelet aggregation. Genetic polymorphisms of P2Y1 and P2Y12 play a major role in the variation of ADP-induced platelet aggregation and in response in antiplatelet therapy. Objective To evaluate the allele frequencies of P2Y1 and P2Y12 genetic polymorphisms in a Korean population and to assess their role in ADP (5 μmol/L)-induced maximal platelet aggregation. Methods P2Y1 (c.1622A > G) and P2Y12 (i-139C > T, i-744 T > C, i-ins801, c.52G > T, c.34C > T) polymorphisms were analyzed in 158 Korean healthy participants using pyrosequencing methods. Their ADP-induced maximal platelet aggregation was assessed by the turbidometric method. Results The observed allele frequencies of P2Y1 and P2Y12 were as follows: 0.3101 for P2Y1 c.1622A > G; 0.1804 for P2Y12 i-139C > T, 0.1804 for i-744 T > C, 0.1804 for i-801insA, 0.1266 for P2Y12 c.52G > T, and 0.2658 for P2Y12 c.34C > T. ADP-induced maximal platelet aggregation was not influenced by the P2Y 1 c.1622A > G polymorphism and was also not affected by three intronic P2Y12 polymorphisms and the P2Y12 c.34C > T polymorphism. However, the P2Y12 c.52G > T polymorphism caused a substantial difference in ADP-induced maximal platelet aggregation (62.75{\%} for c.52GG, 66.27{\%} for c.52GT, and 80.60{\%} for c.52TT; P = 0.0092). Conclusions The P2Y1 and P2Y12 genes were very polymorphic in a Korean population. Three intronic P2Y12 polymorphisms (i-139C > T, i-744 T > C, i-801insA) were in complete linkage disequilibrium but not with the c.52C > T polymorphism in this population. Maximal platelet aggregation in response to ADP is associated with the c.52C > T polymorphism but not with the three intronic polymorphisms or the P2Y1 c.1622A > T polymorphism.",
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T1 - Effect of P2Y1 and P2Y12 genetic polymorphisms on the ADP-induced platelet aggregation in a Korean population

AU - Kim, Kyoung Ah

AU - Song, Wan Geun

AU - Lee, Hye Mi

AU - Joo, Hyun Jin

AU - Park, Ji-Young

PY - 2013/8/1

Y1 - 2013/8/1

N2 - Background P2Y1 and P2Y12 receptors are expressed in platelet membranes and are involved in ADP-induced platelet aggregation. Genetic polymorphisms of P2Y1 and P2Y12 play a major role in the variation of ADP-induced platelet aggregation and in response in antiplatelet therapy. Objective To evaluate the allele frequencies of P2Y1 and P2Y12 genetic polymorphisms in a Korean population and to assess their role in ADP (5 μmol/L)-induced maximal platelet aggregation. Methods P2Y1 (c.1622A > G) and P2Y12 (i-139C > T, i-744 T > C, i-ins801, c.52G > T, c.34C > T) polymorphisms were analyzed in 158 Korean healthy participants using pyrosequencing methods. Their ADP-induced maximal platelet aggregation was assessed by the turbidometric method. Results The observed allele frequencies of P2Y1 and P2Y12 were as follows: 0.3101 for P2Y1 c.1622A > G; 0.1804 for P2Y12 i-139C > T, 0.1804 for i-744 T > C, 0.1804 for i-801insA, 0.1266 for P2Y12 c.52G > T, and 0.2658 for P2Y12 c.34C > T. ADP-induced maximal platelet aggregation was not influenced by the P2Y 1 c.1622A > G polymorphism and was also not affected by three intronic P2Y12 polymorphisms and the P2Y12 c.34C > T polymorphism. However, the P2Y12 c.52G > T polymorphism caused a substantial difference in ADP-induced maximal platelet aggregation (62.75% for c.52GG, 66.27% for c.52GT, and 80.60% for c.52TT; P = 0.0092). Conclusions The P2Y1 and P2Y12 genes were very polymorphic in a Korean population. Three intronic P2Y12 polymorphisms (i-139C > T, i-744 T > C, i-801insA) were in complete linkage disequilibrium but not with the c.52C > T polymorphism in this population. Maximal platelet aggregation in response to ADP is associated with the c.52C > T polymorphism but not with the three intronic polymorphisms or the P2Y1 c.1622A > T polymorphism.

AB - Background P2Y1 and P2Y12 receptors are expressed in platelet membranes and are involved in ADP-induced platelet aggregation. Genetic polymorphisms of P2Y1 and P2Y12 play a major role in the variation of ADP-induced platelet aggregation and in response in antiplatelet therapy. Objective To evaluate the allele frequencies of P2Y1 and P2Y12 genetic polymorphisms in a Korean population and to assess their role in ADP (5 μmol/L)-induced maximal platelet aggregation. Methods P2Y1 (c.1622A > G) and P2Y12 (i-139C > T, i-744 T > C, i-ins801, c.52G > T, c.34C > T) polymorphisms were analyzed in 158 Korean healthy participants using pyrosequencing methods. Their ADP-induced maximal platelet aggregation was assessed by the turbidometric method. Results The observed allele frequencies of P2Y1 and P2Y12 were as follows: 0.3101 for P2Y1 c.1622A > G; 0.1804 for P2Y12 i-139C > T, 0.1804 for i-744 T > C, 0.1804 for i-801insA, 0.1266 for P2Y12 c.52G > T, and 0.2658 for P2Y12 c.34C > T. ADP-induced maximal platelet aggregation was not influenced by the P2Y 1 c.1622A > G polymorphism and was also not affected by three intronic P2Y12 polymorphisms and the P2Y12 c.34C > T polymorphism. However, the P2Y12 c.52G > T polymorphism caused a substantial difference in ADP-induced maximal platelet aggregation (62.75% for c.52GG, 66.27% for c.52GT, and 80.60% for c.52TT; P = 0.0092). Conclusions The P2Y1 and P2Y12 genes were very polymorphic in a Korean population. Three intronic P2Y12 polymorphisms (i-139C > T, i-744 T > C, i-801insA) were in complete linkage disequilibrium but not with the c.52C > T polymorphism in this population. Maximal platelet aggregation in response to ADP is associated with the c.52C > T polymorphism but not with the three intronic polymorphisms or the P2Y1 c.1622A > T polymorphism.

KW - ADP

KW - P2Y

KW - P2Y

KW - Platelet aggregation

KW - Polymorphism

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