Racial differences in human platelet PAR4 reactivity reflect expression of PCTP and miR-376c

In exploring the possibility that racial differences in platelet function might exist, Paul Bray and his colleagues report that platelets from blacks have a greater propensity to aggregate than those from whites in response to activation of the PAR4 thrombin receptor. Mechanistically, this differenc...

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Vydané v:	Nature medicine Ročník 19; číslo 12; s. 1609 - 1616
Hlavní autori:	Edelstein, Leonard C, Simon, Lukas M, Montoya, Raúl Teruel, Holinstat, Michael, Chen, Edward S, Bergeron, Angela, Kong, Xianguo, Nagalla, Srikanth, Mohandas, Narla, Cohen, David E, Dong, Jing-fei, Shaw, Chad, Bray, Paul F
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	New York Nature Publishing Group US 01.12.2013 Nature Publishing Group
Predmet:	13/89 14/19 38/39 38/61 38/77 38/90 692/308/2056 692/699/75/567 82/29 82/80 96/1 96/106 96/109 96/31 96/34 96/63 Atherosclerosis Biomedicine Blood platelets Blood Platelets - metabolism Calcium Cancer Research Carrier proteins Cell receptors Cells, Cultured Continental Population Groups - genetics Demographic aspects Embolism, Cholesterol - ethnology Embolism, Cholesterol - genetics Embolism, Cholesterol - metabolism Gene expression Genetic aspects HCT116 Cells Hep G2 Cells Humans Identification and classification Infectious Diseases Metabolic Diseases MicroRNAs - genetics Molecular Medicine Neurosciences Phospholipid Transfer Proteins - genetics Phospholipid Transfer Proteins - metabolism Platelet Aggregation - genetics Racial differences Receptors, Thrombin - metabolism Studies Thrombolytic drugs Thrombosis - ethnology Thrombosis - genetics Thrombosis - metabolism United States > US
ISSN:	1078-8956, 1546-170X, 1546-170X
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Abstract	In exploring the possibility that racial differences in platelet function might exist, Paul Bray and his colleagues report that platelets from blacks have a greater propensity to aggregate than those from whites in response to activation of the PAR4 thrombin receptor. Mechanistically, this difference in platelet function seems to reflect differences in the expression of the microRNA miR-376c and its target, the enzyme phosphatidylcholine transfer protein. Racial differences in the pathophysiology of atherothrombosis are poorly understood. We explored the function and transcriptome of platelets in healthy black ( n = 70) and white ( n = 84) subjects. Platelet aggregation and calcium mobilization induced by the PAR4 thrombin receptor were significantly greater in black subjects. Numerous differentially expressed RNAs were associated with both race and PAR4 reactivity, including PCTP (encoding phosphatidylcholine transfer protein), and platelets from black subjects expressed higher levels of PC-TP protein. PC-TP inhibition or depletion blocked PAR4- but not PAR1-mediated activation of platelets and megakaryocytic cell lines. miR-376c levels were differentially expressed by race and PAR4 reactivity and were inversely correlated with PCTP mRNA levels, PC-TP protein levels and PAR4 reactivity. miR-376c regulated the expression of PC-TP in human megakaryocytes. A disproportionately high number of microRNAs that were differentially expressed by race and PAR4 reactivity, including miR-376c , are encoded in the DLK1-DIO3 locus and were expressed at lower levels in platelets from black subjects. These results suggest that PC-TP contributes to the racial difference in PAR4-mediated platelet activation, indicate a genomic contribution to platelet function that differs by race and emphasize a need to consider the effects of race when developing anti-thrombotic drugs.
AbstractList	Racial differences in the pathophysiology of atherothrombosis are poorly understood. We explored the function and transcriptome of platelets in healthy black (n = 70) and white (n = 84) subjects. Platelet aggregation and calcium mobilization induced by the PAR4 thrombin receptor were significantly greater in black subjects. Numerous differentially expressed RNAs were associated with both race and PAR4 reactivity, including PCTP (encoding phosphatidylcholine transfer protein), and platelets from black subjects expressed higher levels of PC-TP protein. PC-TP inhibition or depletion blocked PAR4- but not PAR1-mediated activation of platelets and megakaryocytic cell lines. miR-376c levels were differentially expressed by race and PAR4 reactivity and were inversely correlated with PCTP mRNA levels, PC-TP protein levels and PAR4 reactivity. miR-376c regulated the expression of PC-TP in human megakaryocytes. A disproportionately high number of microRNAs that were differentially expressed by race and PAR4 reactivity, including miR-376c, are encoded in the DLK1-DIO3 locus and were expressed at lower levels in platelets from black subjects. These results suggest that PC-TP contributes to the racial difference in PAR4-mediated platelet activation, indicate a genomic contribution to platelet function that differs by race and emphasize a need to consider the effects of race when developing anti-thrombotic drugs.Racial differences in the pathophysiology of atherothrombosis are poorly understood. We explored the function and transcriptome of platelets in healthy black (n = 70) and white (n = 84) subjects. Platelet aggregation and calcium mobilization induced by the PAR4 thrombin receptor were significantly greater in black subjects. Numerous differentially expressed RNAs were associated with both race and PAR4 reactivity, including PCTP (encoding phosphatidylcholine transfer protein), and platelets from black subjects expressed higher levels of PC-TP protein. PC-TP inhibition or depletion blocked PAR4- but not PAR1-mediated activation of platelets and megakaryocytic cell lines. miR-376c levels were differentially expressed by race and PAR4 reactivity and were inversely correlated with PCTP mRNA levels, PC-TP protein levels and PAR4 reactivity. miR-376c regulated the expression of PC-TP in human megakaryocytes. A disproportionately high number of microRNAs that were differentially expressed by race and PAR4 reactivity, including miR-376c, are encoded in the DLK1-DIO3 locus and were expressed at lower levels in platelets from black subjects. These results suggest that PC-TP contributes to the racial difference in PAR4-mediated platelet activation, indicate a genomic contribution to platelet function that differs by race and emphasize a need to consider the effects of race when developing anti-thrombotic drugs. In exploring the possibility that racial differences in platelet function might exist, Paul Bray and his colleagues report that platelets from blacks have a greater propensity to aggregate than those from whites in response to activation of the PAR4 thrombin receptor. Mechanistically, this difference in platelet function seems to reflect differences in the expression of the microRNA miR-376c and its target, the enzyme phosphatidylcholine transfer protein. Racial differences in the pathophysiology of atherothrombosis are poorly understood. We explored the function and transcriptome of platelets in healthy black ( n = 70) and white ( n = 84) subjects. Platelet aggregation and calcium mobilization induced by the PAR4 thrombin receptor were significantly greater in black subjects. Numerous differentially expressed RNAs were associated with both race and PAR4 reactivity, including PCTP (encoding phosphatidylcholine transfer protein), and platelets from black subjects expressed higher levels of PC-TP protein. PC-TP inhibition or depletion blocked PAR4- but not PAR1-mediated activation of platelets and megakaryocytic cell lines. miR-376c levels were differentially expressed by race and PAR4 reactivity and were inversely correlated with PCTP mRNA levels, PC-TP protein levels and PAR4 reactivity. miR-376c regulated the expression of PC-TP in human megakaryocytes. A disproportionately high number of microRNAs that were differentially expressed by race and PAR4 reactivity, including miR-376c , are encoded in the DLK1-DIO3 locus and were expressed at lower levels in platelets from black subjects. These results suggest that PC-TP contributes to the racial difference in PAR4-mediated platelet activation, indicate a genomic contribution to platelet function that differs by race and emphasize a need to consider the effects of race when developing anti-thrombotic drugs. Racial differences in the pathophysiology of atherothrombosis are poorly understood. We explored the function and transcriptome of platelets in healthy black (n = 70) and white (n = 84) subjects. Platelet aggregation and calcium mobilization induced by the PAR4 thrombin receptor were significantly greater in black subjects. Numerous differentially expressed RNAs were associated with both race and PAR4 reactivity, including PCTP (encoding phosphatidylcholine transfer protein), and platelets from black subjects expressed higher levels of PC-TP protein. PC-TP inhibition or depletion blocked PAR4- but not PAR1-mediated activation of platelets and megakaryocytic cell lines. miR-376c levels were differentially expressed by race and PAR4 reactivity and were inversely correlated with PCTP mRNA levels, PC-TP protein levels and PAR4 reactivity. miR-376c regulated the expression of PC-TP in human megakaryocytes. A disproportionately high number of microRNAs that were differentially expressed by race and PAR4 reactivity, including miR-376c, are encoded in the DLK1-DIO3 locus and were expressed at lower levels in platelets from black subjects. These results suggest that PC-TP contributes to the racial difference in PAR4-mediated platelet activation, indicate a genomic contribution to platelet function that differs by race and emphasize a need to consider the effects of race when developing anti-thrombotic drugs.
Audience	Academic
Author	Bergeron, Angela Nagalla, Srikanth Edelstein, Leonard C Simon, Lukas M Shaw, Chad Kong, Xianguo Montoya, Raúl Teruel Holinstat, Michael Cohen, David E Dong, Jing-fei Bray, Paul F Mohandas, Narla Chen, Edward S
Author_xml	– sequence: 1 givenname: Leonard C surname: Edelstein fullname: Edelstein, Leonard C organization: The Cardeza Foundation for Hematologic Research and Department of Medicine, Jefferson Medical College, Thomas Jefferson University – sequence: 2 givenname: Lukas M surname: Simon fullname: Simon, Lukas M organization: Department of Molecular and Human Genetics, Baylor College of Medicine – sequence: 3 givenname: Raúl Teruel surname: Montoya fullname: Montoya, Raúl Teruel organization: The Cardeza Foundation for Hematologic Research and Department of Medicine, Jefferson Medical College, Thomas Jefferson University – sequence: 4 givenname: Michael surname: Holinstat fullname: Holinstat, Michael organization: The Cardeza Foundation for Hematologic Research and Department of Medicine, Jefferson Medical College, Thomas Jefferson University – sequence: 5 givenname: Edward S surname: Chen fullname: Chen, Edward S organization: Department of Molecular and Human Genetics, Baylor College of Medicine – sequence: 6 givenname: Angela surname: Bergeron fullname: Bergeron, Angela organization: Department of Medicine, Baylor College of Medicine – sequence: 7 givenname: Xianguo surname: Kong fullname: Kong, Xianguo organization: The Cardeza Foundation for Hematologic Research and Department of Medicine, Jefferson Medical College, Thomas Jefferson University – sequence: 8 givenname: Srikanth surname: Nagalla fullname: Nagalla, Srikanth organization: The Cardeza Foundation for Hematologic Research and Department of Medicine, Jefferson Medical College, Thomas Jefferson University – sequence: 9 givenname: Narla surname: Mohandas fullname: Mohandas, Narla organization: New York Blood Center – sequence: 10 givenname: David E surname: Cohen fullname: Cohen, David E organization: Department of Medicine, Division of Gastroenterology, Brigham and Women's Hospital, Harvard Medical School – sequence: 11 givenname: Jing-fei surname: Dong fullname: Dong, Jing-fei organization: Puget Sound Blood Center – sequence: 12 givenname: Chad surname: Shaw fullname: Shaw, Chad email: cashaw@bcm.tmc.edu organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Department of Statistics, Rice University – sequence: 13 givenname: Paul F surname: Bray fullname: Bray, Paul F email: paul.bray@jefferson.edu organization: The Cardeza Foundation for Hematologic Research and Department of Medicine, Jefferson Medical College, Thomas Jefferson University
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/24216752$$D View this record in MEDLINE/PubMed
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Snippet	In exploring the possibility that racial differences in platelet function might exist, Paul Bray and his colleagues report that platelets from blacks have a... Racial differences in the pathophysiology of atherothrombosis are poorly understood. We explored the function and transcriptome of platelets in healthy black...
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SubjectTerms	13/89 14/19 38/39 38/61 38/77 38/90 692/308/2056 692/699/75/567 82/29 82/80 96/1 96/106 96/109 96/31 96/34 96/63 Atherosclerosis Biomedicine Blood platelets Blood Platelets - metabolism Calcium Cancer Research Carrier proteins Cell receptors Cells, Cultured Continental Population Groups - genetics Demographic aspects Embolism, Cholesterol - ethnology Embolism, Cholesterol - genetics Embolism, Cholesterol - metabolism Gene expression Genetic aspects HCT116 Cells Hep G2 Cells Humans Identification and classification Infectious Diseases Metabolic Diseases MicroRNAs - genetics Molecular Medicine Neurosciences Phospholipid Transfer Proteins - genetics Phospholipid Transfer Proteins - metabolism Platelet Aggregation - genetics Racial differences Receptors, Thrombin - metabolism Studies Thrombolytic drugs Thrombosis - ethnology Thrombosis - genetics Thrombosis - metabolism
Title	Racial differences in human platelet PAR4 reactivity reflect expression of PCTP and miR-376c
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