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Article ; Online: Sources of variability in the human platelet transcriptome.

Thibord, Florian / Johnson, Andrew D

2023 Volume 231, Page(s) 255–263

Abstract: Platelets are anucleated cells produced by megakaryocytes, from which they inherit all the components necessary to carry their functions. They circulate in blood vessels where they play essential roles in coagulation, wound repair or inflammation, and ... ...

Abstract	Platelets are anucleated cells produced by megakaryocytes, from which they inherit all the components necessary to carry their functions. They circulate in blood vessels where they play essential roles in coagulation, wound repair or inflammation, and have been implicated in various pathological conditions such as thrombosis, viral infection or cancer progression. The importance of these cells has been established over a century ago, and effective anti-platelet medications with different mechanisms of action have since been developed. However, these therapies are not always effective and can incur adverse events, thus a better understanding of platelets molecular processes is needed to address these issues and improve our understanding of platelet functions. In recent years, an increasing number of studies have leveraged OMICs technologies to analyze their content and identify molecular signatures and mechanisms associated with platelet functions and platelet related disorders. In particular, the increased accessibility of microarrays and RNA sequencing opened the way for studies of the platelet transcriptome under a wide array of conditions. These studies revealed distinct expression profiles in diverse pathologies, which could lead to the discovery of novel biomarkers and therapeutic targets, and suggests a dynamic transcriptome that could influence platelet mechanisms. In this review, we highlight the different sources of transcript level variability in platelets while summarizing recent advances and discoveries from this emerging field.
MeSH term(s)	Humans ; Transcriptome ; Blood Platelets/metabolism ; Megakaryocytes ; Blood Coagulation ; Hemostasis ; Blood Platelet Disorders
Language	English
Publishing date	2023-06-16
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	121852-9
ISSN	1879-2472 ; 0049-3848
ISSN (online)	1879-2472
ISSN	0049-3848
DOI	10.1016/j.thromres.2023.06.009
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Article ; Online: A year of COVID-19 GWAS results from the GRASP portal reveals potential genetic risk factors.

Thibord, Florian / Chan, Melissa V / Chen, Ming-Huei / Johnson, Andrew D

HGG advances

2022 Volume 3, Issue 2, Page(s) 100095

Abstract: Host genetic variants influence the susceptibility and severity of several infectious diseases, and the discovery of genetic associations with coronavirus disease 2019 (COVID-19) phenotypes could help to develop new therapeutic strategies to decrease its ...

Abstract	Host genetic variants influence the susceptibility and severity of several infectious diseases, and the discovery of genetic associations with coronavirus disease 2019 (COVID-19) phenotypes could help to develop new therapeutic strategies to decrease its burden. Between May 2020 and June 2021, we used COVID-19 data released periodically by UK Biobank and performed 65 genome-wide association studies in up to 18 releases of COVID-19 susceptibility (n = 18,481 cases in June 2021), hospitalization (n = 3,260), severe outcomes (n = 1,244), and deaths (n = 1,104), stratified by sex and ancestry. In coherence with previous studies, we observed two independent signals at the chr3p21.31 locus (rs73062389-A, odds ratio [OR], 1.21 (P = 4.26 × 10
Language	English
Publishing date	2022-02-22
Publishing country	United States
Document type	Journal Article
ISSN	2666-2477
ISSN (online)	2666-2477
DOI	10.1016/j.xhgg.2022.100095
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Article ; Online: The association between platelet reactivity and lipoprotein levels in Framingham Heart Study participants.

Nkambule, Bongani Brian / Chan, Melissa Victoria / Lachapelle, Amber Rose / Grech, Joseph / Thibord, Florian / Chen, Ming-Huei / Johnson, Andrew Danner

Thrombosis research

2023 Volume 225, Page(s) 103–109

Abstract: Background: Hypertriglyceridemia is an independent risk factor for major adverse cardiovascular events, though the mechanisms linking triglycerides and platelet function with thrombosis, remain elusive. The aim of this study was to assess the ... ...

Abstract	Background: Hypertriglyceridemia is an independent risk factor for major adverse cardiovascular events, though the mechanisms linking triglycerides and platelet function with thrombosis, remain elusive. The aim of this study was to assess the association between platelet function and triglyceride levels. Methods: We included participants from the Framingham Heart Study Third Generation cohort, OMNI, and New Offspring Spouse cohort who attended the third examination cycle (2016-2019). Eligible participants were categorized into four triglyceride subgroups. Results: The study comprised a total of 1897 (55.53 %) participants with normal TG levels; 883 (25.85 %) participants with high-normal TGs; 378 (11.07 %) with borderline high TGs; and 258 (7.55 %) participants with hypertriglyceridemia. After adjusting for age, sex, alcohol consumption, aspirin, statin and P2Y Conclusion: Triglyceride levels are associated with altered platelet activation and aggregation. Furthermore, increased platelet-driven thrombogenicity is directly associated with triglyceride levels after adjusting for medications and other covariates.
MeSH term(s)	Humans ; Triglycerides/therapeutic use ; Lipoproteins, LDL ; Longitudinal Studies ; Hypertriglyceridemia/drug therapy ; Cholesterol
Chemical Substances	Triglycerides ; Lipoproteins, LDL ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2023-03-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	121852-9
ISSN	1879-2472 ; 0049-3848
ISSN (online)	1879-2472
ISSN	0049-3848
DOI	10.1016/j.thromres.2023.03.013
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Article ; Online: Alcohol intake including wine drinking is associated with decreased platelet reactivity in a large population sample.

Pashek, Robin E / Nkambule, Bongani B / Chan, Melissa V / Thibord, Florian / Lachapelle, Amber R / Cunha, Jason / Chen, Ming-Huei / Johnson, Andrew D

International journal of epidemiology

2023 Volume 52, Issue 6, Page(s) 1939–1950

Abstract: Background: Alcohol consumption is linked to decreased platelet function. Whether this link is dependent on sex or type of beverage remains unclear.: Methods: Cross-sectional data were obtained from the Framingham Heart Study (N = 3427). Alcohol ... ...

Abstract	Background: Alcohol consumption is linked to decreased platelet function. Whether this link is dependent on sex or type of beverage remains unclear. Methods: Cross-sectional data were obtained from the Framingham Heart Study (N = 3427). Alcohol consumption was assessed by using standardized medical history and Harvard semi-quantitative food frequency questionnaires. Five bioassays measured 120 platelet reactivity traits across agonists in whole-blood and platelet-rich plasma samples. Linear mixed-effects models adjusted for age, sex and aspirin use, hypertension, body mass index, cholesterol, high-density lipoprotein, triglycerides, smoking and diabetes evaluated associations between platelet reactivity and alcohol consumption. Beta effects, the regression coefficients that estimate the amount of change in each unit of the predictor variable whereas all other predictor variables remain fixed, for heavy alcohol consumption were compared with effects of aspirin use. Results: Alcohol consumption was associated with decreased platelet reactivity, with more associations among wine and liquor compared with beer. Many platelet-alcohol associations in the full sample (86%, P < 0.01) had larger effect sizes in females. Lower light transmission aggregometry adenosine diphosphate (1.82 µM) maximum aggregation (P = 2.6E-3, 95% CI = -0.07, -0.02, β = -0.042) and area under the curve (P = 7.7E-3, 95% CI = -0.07, -0.01, β = -0.039) were associated with white wine consumption; however, red wine had no associations with platelet reactivity. The effect of aspirin use was on average 11.3 (±4.0) times greater than that of heavy drinking in our full sample. Conclusions: We confirm associations between alcohol consumption and decreased platelet reactivity. Effects appeared larger for liquor and wine intake and in our female cohort. Red wine consumption is not associated with lower platelet function, contrasting with prior population studies. Although we report an inhibitory relationship between alcohol intake and platelet function, these effects appear much smaller than that of aspirin use.
MeSH term(s)	Humans ; Female ; Wine ; Cross-Sectional Studies ; Alcohol Drinking/epidemiology ; Alcoholic Beverages ; Beer ; Aspirin
Chemical Substances	Aspirin (R16CO5Y76E)
Language	English
Publishing date	2023-08-04
Publishing country	England
Document type	Journal Article
ZDB-ID	187909-1
ISSN	1464-3685 ; 0300-5771
ISSN (online)	1464-3685
ISSN	0300-5771
DOI	10.1093/ije/dyad099
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Article ; Online: Trends among platelet function, arterial calcium, and vascular function measures.

Cunha, Jason / Chan, Melissa V / Nkambule, Bongani B / Thibord, Florian / Lachapelle, Amber / Pashek, Robin E / Vasan, Ramachandran S / Rong, Jian / Benjamin, Emelia J / Hamburg, Naomi M / Chen, Ming-Huei / Mitchell, Gary F / Johnson, Andrew D

Platelets

2023 Volume 34, Issue 1, Page(s) 2238835

Abstract: Arterial tonometry and vascular calcification measures are useful in cardiovascular disease (CVD) risk assessment. Prior studies found associations between tonometry measures, arterial calcium, and CVD risk. Activated platelets release angiopoietin-1 and ...

Abstract	Arterial tonometry and vascular calcification measures are useful in cardiovascular disease (CVD) risk assessment. Prior studies found associations between tonometry measures, arterial calcium, and CVD risk. Activated platelets release angiopoietin-1 and other factors, which may connect vascular structure and platelet function. We analyzed arterial tonometry, platelet function, aortic, thoracic and coronary calcium, and thoracic and abdominal aorta diameters measured in the Framingham Heart Study Gen3/NOS/OMNI-2 cohorts (
MeSH term(s)	Female ; Male ; Humans ; Calcium ; Pulse Wave Analysis ; Blood Pressure ; Platelet Activation ; Atherosclerosis
Chemical Substances	Calcium (SY7Q814VUP)
Language	English
Publishing date	2023-08-24
Publishing country	England
Document type	Journal Article
ZDB-ID	1034283-7
ISSN	1369-1635 ; 0953-7104
ISSN (online)	1369-1635
ISSN	0953-7104
DOI	10.1080/09537104.2023.2238835
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Article ; Online: A year of COVID-19 GWAS results from the GRASP portal reveals potential SARS-CoV-2 modifiers

Thibord, Florian / Chan, Melissa V. / Chen, Ming-Huei / Johnson, Andrew D.

medRxiv

Abstract: Host genetic variants influence the susceptibility and severity of several infectious diseases, and the discovery of novel genetic associations with Covid-19 phenotypes could help developing new therapeutic strategies to reduce its burden. Between May ... ...

Abstract	Host genetic variants influence the susceptibility and severity of several infectious diseases, and the discovery of novel genetic associations with Covid-19 phenotypes could help developing new therapeutic strategies to reduce its burden. Between May 2020 and February 2021, we used Covid-19 data released periodically by UK Biobank and performed over 400 Genome-Wide Association Studies (GWAS) of Covid-19 susceptibility (N=15,738 cases), hospitalization (N=1,916), severe outcomes (N=935) and death (N=828), stratified by ancestry and sex. In coherence with previous studies, we observed 2 independent signals at the chr3p21.31 locus (rs73062389-A, OR=1.22, P=7.64E-14 and rs13092887-A, OR=1.73, P=2.38E-8, in Europeans) modulating susceptibility and severity, respectively, and a signal influencing susceptibility at the ABO locus (rs9411378-A, OR=1.10, P =7.36E-10, in Europeans), which was more significant in men than in women (P=0.01). In addition, we detected 7 genome-wide significant signals in the last data release analyzed (on February 24th 2021), of which 4 were associated with susceptibility (SCRT2, LRMDA, chr15q24.2, MIR3681HG), 2 with hospitalization (ANKS1A, chr12p13.31) and 1 for severity (ADGRE1). Finally, we identified over 300 associations which increased in significance over time, and reached at least P<10-5 in the last data release analyzed. We replicated 2 of these signals in an independent dataset: a variant downstream of CCL3 (rs2011959) associated with severity in men, and a variant located in an ATP5PO intron (rs12482569) associated with hospitalization. These results, freely available on the GRASP portal, provide new insights on the host genetic architecture of Covid-19 phenotypes.
Keywords	covid19
Language	English
Publishing date	2021-06-11
Publisher	Cold Spring Harbor Laboratory Press
Document type	Article ; Online
DOI	10.1101/2021.06.08.21258507
Database	COVID19

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Article ; Online: Genetic and nongenetic drivers of platelet reactivity in healthy Tanzanian individuals.

Kullaya, Vesla I / Temba, Godfrey S / Vadaq, Nadira / Njau, Judith / Boahen, Collins K / Nkambule, Bongani B / Thibord, Florian / Chen, Ming-Huei / Pecht, Tal / Lyamuya, Furaha / Kumar, Vinod / Netea, Mihai G / Mmbaga, Blandina T / van der Ven, Andre / Johnson, Andrew D / de Mast, Quirijn

Journal of thrombosis and haemostasis : JTH

2023 Volume 22, Issue 3, Page(s) 805–817

Abstract: Background: Platelets play a key role in hemostasis, inflammation, and cardiovascular diseases. Platelet reactivity is highly variable between individuals. The drivers of this variability in populations from Sub-Saharan Africa remain largely unknown.: ...

Abstract	Background: Platelets play a key role in hemostasis, inflammation, and cardiovascular diseases. Platelet reactivity is highly variable between individuals. The drivers of this variability in populations from Sub-Saharan Africa remain largely unknown. Objectives: We aimed to investigate the nongenetic and genetic determinants of platelet reactivity in healthy adults living in a rapidly urbanizing area in Northern Tanzania. Methods: Platelet activation and reactivity were measured by platelet P-selectin expression and the binding of fibrinogen in unstimulated blood and after ex vivo stimulation with adenosine diphosphate and PAR-1 and PAR-4 ligands. We then analyzed the associations of platelet parameters with host genetic and nongenetic factors, environmental factors, plasma inflammatory markers, and plasma metabolites. Results: Only a few associations were found between platelet reactivity parameters and plasma inflammatory markers and nongenetic host and environmental factors. In contrast, untargeted plasma metabolomics revealed a large number of associations with food-derived metabolites, including phytochemicals that were previously reported to inhibit platelet reactivity. Genome-wide single-nucleotide polymorphism genotyping identified 2 novel single-nucleotide polymorphisms (rs903650 and rs4789332) that were associated with platelet reactivity at the genome-wide level (P < 5 × 10 Conclusion: Our study uncovered factors that determine variation in platelet reactivity in a population in East Africa that is rapidly transitioning to an urban lifestyle, including the importance of genetic ancestry and the gradual abandoning of the traditional East African diet.
MeSH term(s)	Adult ; Humans ; Platelet Aggregation/physiology ; Tanzania ; Blood Platelets/metabolism ; Platelet Activation ; Receptor, PAR-1/metabolism
Chemical Substances	Receptor, PAR-1
Language	English
Publishing date	2023-11-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1016/j.jtha.2023.11.014
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Zs.A 5805: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 295: Show issues

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Article: Causal relationships between risk of venous thromboembolism and 18 cancers: a bidirectional Mendelian randomisation analysis.

Cornish, Naomi / Haycock, Philip / Brenner, Hermann / Figueiredo, Jane C / Galesloot, Tessel / Grant, Robert C / Johansson, Mattias / Mariosa, Daniela / McKay, James / Pai, Rish / Pellatt, Andrew J / Samadder, N Jewel / Shi, Jianxin / Thibord, Florian / Trégouët, David-Alexandre / Voegele, Catherine / Thirlwell, Chrissie / Mumford, Andrew / Langdon, Ryan

medRxiv : the preprint server for health sciences

2023

Abstract: Background: People with cancer experience high rates of venous thromboembolism (VTE). Additionally, risk of subsequent cancer is increased in people experiencing their first VTE. The causal mechanisms underlying this association are not completely ... ...

Abstract	Background: People with cancer experience high rates of venous thromboembolism (VTE). Additionally, risk of subsequent cancer is increased in people experiencing their first VTE. The causal mechanisms underlying this association are not completely understood, and it is unknown whether VTE is itself a risk factor for cancer. Methods: We used data from large genome-wide association study meta-analyses to perform bi-directional Mendelian randomisation analyses to estimate causal associations between genetically-proxied lifetime risk of VTE and risk of 18 different cancers. Results: We found no conclusive evidence that genetically-proxied lifetime risk of VTE was causally associated with an increased incidence of cancer, or vice-versa. We observed an association between VTE and pancreatic cancer risk (odds ratio for pancreatic cancer 1.23 (95% confidence interval 1.08 - 1.40) per log-odds increase in risk of VTE, Conclusions: These findings do not support the hypothesis that genetically-proxied lifetime risk of VTE is a cause of cancer. Existing observational epidemiological associations between VTE and cancer are therefore more likely to be driven by pathophysiological changes which occur in the setting of active cancer and anti-cancer treatments. Further work is required to explore and synthesise evidence for these mechanisms.
Language	English
Publishing date	2023-05-18
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.16.23289792
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Article: Multi-ancestry polygenic risk scores for venous thromboembolism.

Jee, Yon Ho / Thibord, Florian / Dominguez, Alicia / Sept, Corriene / Boulier, Kristin / Venkateswaran, Vidhya / Ding, Yi / Cherlin, Tess / Verma, Shefali Setia / Faro, Valeria Lo / Bartz, Traci M / Boland, Anne / Brody, Jennifer A / Deleuze, Jean-Francois / Emmerich, Joseph / Germain, Marine / Johnson, Andrew D / Kooperberg, Charles / Morange, Pierre-Emmanuel /

Pankratz, Nathan / Psaty, Bruce M / Reiner, Alexander P / Smadja, David M / Sitlani, Colleen M / Suchon, Pierre / Tang, Weihong / Trégouët, David-Alexandre / Zöllner, Sebastian / Pasaniuc, Bogdan / Damrauer, Scott M / Sanna, Serena / Snieder, Harold / Kabrhel, Christopher / Smith, Nicholas L / Kraft, Peter

medRxiv : the preprint server for health sciences

2024

Abstract: Venous thromboembolism (VTE) is a significant contributor to morbidity and mortality, with large disparities in incidence rates between Black and White Americans. Polygenic risk scores (PRSs) limited to variants discovered in genome-wide association ... ...

Abstract	Venous thromboembolism (VTE) is a significant contributor to morbidity and mortality, with large disparities in incidence rates between Black and White Americans. Polygenic risk scores (PRSs) limited to variants discovered in genome-wide association studies in European-ancestry samples can identify European-ancestry individuals at high risk of VTE. However, there is limited evidence on whether high-dimensional PRS constructed using more sophisticated methods and more diverse training data can enhance the predictive ability and their utility across diverse populations. We developed PRSs for VTE using summary statistics from the International Network against Venous Thrombosis (INVENT) consortium GWAS meta-analyses of European- (71,771 cases and 1,059,740 controls) and African-ancestry samples (7,482 cases and 129,975 controls). We used LDpred2 and PRSCSx to construct ancestry-specific and multi-ancestry PRSs and evaluated their performance in an independent European- (6,261 cases and 88,238 controls) and African-ancestry sample (1,385 cases and 12,569 controls). Multi-ancestry PRSs with weights tuned in European- and African-ancestry samples, respectively, outperformed ancestry-specific PRSs in European- (PRSCSX
Language	English
Publishing date	2024-01-10
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.09.24300914
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Article ; Online: Causal relationships between risk of venous thromboembolism and 18 cancers: a bidirectional Mendelian randomization analysis.

Cornish, Naomi / Haycock, Philip / Brenner, Hermann / Figueiredo, Jane C / Galesloot, Tessel E / Grant, Robert C / Johansson, Mattias / Mariosa, Daniela / McKay, James / Pai, Rish / Pellatt, Andrew J / Samadder, N Jewel / Shi, Jianxin / Thibord, Florian / Trégouët, David-Alexandre / Voegele, Catherine / Thirlwell, Chrissie / Mumford, Andrew / Langdon, Ryan

International journal of epidemiology

2023 Volume 53, Issue 1

Abstract: Background: People with cancer experience high rates of venous thromboembolism (VTE). Risk of subsequent cancer is also increased in people experiencing their first VTE. The causal mechanisms underlying this association are not completely understood, ... ...

Abstract	Background: People with cancer experience high rates of venous thromboembolism (VTE). Risk of subsequent cancer is also increased in people experiencing their first VTE. The causal mechanisms underlying this association are not completely understood, and it is unknown whether VTE is itself a risk factor for cancer. Methods: We used data from large genome-wide association study meta-analyses to perform bidirectional Mendelian randomization analyses to estimate causal associations between genetic liability to VTE and risk of 18 different cancers. Results: We found no conclusive evidence that genetic liability to VTE was causally associated with an increased incidence of cancer, or vice versa. We observed an association between liability to VTE and pancreatic cancer risk [odds ratio for pancreatic cancer: 1.23 (95% confidence interval: 1.08-1.40) per log-odds increase in VTE risk, P = 0.002]. However, sensitivity analyses revealed this association was predominantly driven by a variant proxying non-O blood group, with inadequate evidence to suggest a causal relationship. Conclusions: These findings do not support the hypothesis that genetic liability to VTE is a cause of cancer. Existing observational epidemiological associations between VTE and cancer are therefore more likely to be driven by pathophysiological changes which occur in the setting of active cancer and anti-cancer treatments. Further work is required to explore and synthesize evidence for these mechanisms.
MeSH term(s)	Humans ; Venous Thromboembolism/epidemiology ; Venous Thromboembolism/genetics ; Mendelian Randomization Analysis ; Genome-Wide Association Study ; Risk Factors ; Pancreatic Neoplasms/epidemiology ; Pancreatic Neoplasms/genetics
Language	English
Publishing date	2023-12-20
Publishing country	England
Document type	Journal Article
ZDB-ID	187909-1
ISSN	1464-3685 ; 0300-5771
ISSN (online)	1464-3685
ISSN	0300-5771
DOI	10.1093/ije/dyad170
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