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Racial Difference in Human Platelet PAR4 Reactivity Reflects Expression of PCTP and miR-376c

ABSTRACT: 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. Numerous differentially expressed (DE) RNAs were associated with both race and PAR4 reactivity, including phosphatidylcholine transfer protein (PCTP), and platelets from blacks expressed higher levels of PC-TP protein.

ORGANISM(S): Homo sapiens

PROVIDER: GSE49921 | GEO | 2013/11/15

SECONDARY ACCESSION(S): PRJNA215334

REPOSITORIES: GEO

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Racial Difference in Human Platelet PAR4 Reactivity Reflects Expression of PCTP and miR-376c

Project description: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. Numerous differentially expressed (DE) RNAs were associated with both race and PAR4 reactivity, including phosphatidylcholine transfer protein (PCTP), and platelets from blacks expressed higher levels of PC-TP protein. Purified platellets were obtained from 154 healthy volunteers not taking blood thinning medication, suffering from blood diseases or otherwise excluded for health reasons. RNA was extracted and profiled on these subjects. Simultaneously, purified platelets were phenotyped using aggregation in response to stimulation with agonist. The agonist response scores and races as ewll as gene expression values on these individuals are provided.

2013-11-15 | E-GEOD-49921 | biostudies-arrayexpress

Regulatory Role for PC-TP/StarD2 in the Metabolic Response to Peroxisome Proliferator Activated Receptor Alpha (PPARα)

2010-08-12 | GSE17666 | GEO

Regulatory Role for PC-TP/StarD2 in the Metabolic Response to Peroxisome Proliferator Activated Receptor Alpha (PPARα)

Project description:Phosphatidylcholine transfer protein (PC-TP, a.k.a StarD2) is abundantly expressed in liver and is regulated by PPARα. When fed the synthetic PPARα ligand fenofibrate, Pctp-/- mice exhibited altered lipid and glucose homeostasis. Microarray profiling of liver from fenofibrate fed wild type and Pctp-/- mice revealed differential expression of a broad array of metabolic genes, as well as their regulatory transcription factors. Because its expression controlled the transcriptional activities of both PPARα and HNF4α in cell culture, the broader impact of PC-TP on nutrient metabolism is most likely secondary to its role in fatty acid metabolism. 6 livers collected from PC-TP knockout mice fed a fenobrate-supplemented diet were used as the experimental group. 6 livers collected from wild type mice fed a fenofibrate-supplemented diet were used as the control group. RNA prepared from one liver was used to hybridize one GeneChip, so that there were 6 experimental GeneChips and 6 control GeneChips.

2010-08-12 | E-GEOD-17666 | biostudies-arrayexpress

Platelet Reactivity ExpreSsion Score Predicts Cardiovascular Risk

Project description:Platelets are key mediators of atherothrombosis; yet, limited tools exist to identify individuals with a hyperreactive platelet phenotype. Here we derive and validate a Platelet Reactivity ExpreSsion Score (PRESS) integrating platelet aggregation responses and RNA sequencing in multiple cohorts. PRESS performs well in identifying a hyperreactive phenotype in patients with cardiovascular disease (AUC [cross-validation] 0.81, 95% CI 0.68 to 0.94), with similar discrimination in an independent cohort of healthy participants (AUC [validation] 0.77, 95% CI 0.75 to 0.79); accuracy 80%, sensitivity 71%, and specificity 86%. Next, we validate PRESS in multiple cohorts of patients with platelet RNASeq available. Following multivariable adjustment, PRESS was significantly higher in MI (β=1.8, p=0.02), and individuals with a score above the median more frequently develop a future cardiovascular event (adjusted HR 1.90, CI 1.07 to 3.36), p=0.027). Altogether, we provide strong evidence that PRESS is a robust prognostic marker, which could have an essential role in facilitating a personalized approach to cardiovascular risk management.

2024-06-30 | GSE232027 | GEO

Cardiac DNA Methylation Underlies Racial and Socioeconomic Disparities among Patients with End-Stage Heart Failure (RNA-seq)

Project description:African Americans (AA) are 70% more likely than Caucasian Americans (CA) to die from heart failure (HF) even after adjusting for known causes. Although the causal factors responsible for this racial disparity remain unknown, it is theorized that environmental stressors This alarming health disparity represents an important challenge to U.S. healthcare as global prevalence of heart failure has already exceeded epidemic levels with a disease burden that disproportionately impacts members of ethnic and racial minorities. The current multicohort study of cardiac DNA methylation identifies the cardiac epigenome as a previously unrecognized syntax that encodes race-based environmental differences in the failing human heart.

2021-03-11 | GSE164196 | GEO

Cardiac DNA Methylation Underlies Racial and Socioeconomic Disparities among Patients with End-Stage Heart Failure (MethylationEPIC array)

2021-03-11 | GSE164195 | GEO

Homo sapiens

Project description:Racial Difference in Human Platelet PAR4 Reactivity Reflects Expression of PCTP and miR-376c

| PRJNA215334 | ENA

Platelet microRNA-mRNA Co-Expression Profiles Correlate with Platelet Reactivity

Project description:MicroRNAs (miRNAs) regulate cell physiology by altering protein expression, but the biology of platelet miRNAs is largely unexplored. We tested whether platelet miRNA levels were associated with platelet reactivity by genome-wide profiling using platelet RNA from 19 healthy subjects. We found that human platelets express 284 miRNAs. Unsupervised hierarchical clustering of miRNA profiles resulted in 2 groups of subjects that appeared to cluster by platelet aggregation phenotypes. Seventy-four miRNAs were differentially expressed (DE) between subjects grouped according to platelet aggregation to epinephrine, a subset of which predicted the platelet reactivity response. Using whole genome mRNA expression data on these same subjects, we computationally generated a high-priority list of miRNA-mRNA pairs in which the DE platelet miRNAs had binding sites in 3'UTRs of DE mRNAs, and the levels were negatively correlated. Three miRNA-mRNA pairs (miR-200b:PRKAR2B, miR-495:KLHL5 and miR-107:CLOCK) were selected from this list and all 3 miRNAs knocked down protein expression from the target mRNA. Reduced activation from platelets lacking PRKAR2B supported these findings. In summary, (1) platelet miRNAs are able to repress expression of platelet proteins, (2) miRNA profiles are associated with and may predict platelet reactivity, and (3) bioinformatic approaches can successfully identify functional miRNAs in platelets. Total RNA from the platelets of 19 donors was harvested and labeled with Hy3. Reference RNA (a pool of all samples) was labeled with Hy5. This submission represents the miRNA expression component of the study.

2011-09-26 | E-GEOD-27917 | biostudies-arrayexpress

Molecular Dysregulation Underlying Racial Disparity in Hepatocellular Carcinoma (HCC)

Project description:Molecular Dysregulation Underlying Racial Disparity in Hepatocellular Carcinoma (HCC)

| PRJNA928394 | ENA

Understanding determinants of racial disparities in lung cancer incidence

Project description:Understanding determinants of racial disparities in lung cancer incidence

| PRJNA1165824 | ENA