Platelets最新文献

{"title":"Identification of UDP-Glucuronosyltransferase mRNA in human platelets: differential levels in smokers and non-smokers.","authors":"Yazun Jarrar, Mansour Almansour, Dina Abulebdeh, Wesam Nasser, Qais Jarrar, Sara Abudahab, Su-Jun Lee","doi":"10.1080/09537104.2025.2536306","DOIUrl":"10.1080/09537104.2025.2536306","url":null,"abstract":"<p><strong>Background: </strong>UDP-glucuronosyl transferases (UGTs) are major enzymes of phase II drug metabolism, yet their expression in human platelets remains underexplored. Objectives: This study aimed to characterize the mRNA expression profile of UGT isoforms in human platelets and to assess differences between cigarette smokers and nonsmokers.</p><p><strong>Methods: </strong>Total RNA was extracted from platelet-rich plasma (PRP), buffy coat (BC), and liver samples. After reverse transcription, PCR was performed to detect UGT isoforms including UGT1A1, 1A3, 1A4, 1A5, 1A6, 1A7, 1A8, 1A9, 1A10, 2B7, and 2B15. The mRNA levels of UGT1A5 and 2B15 in PRP were quantified and compared to levels in liver and BC. PRP samples from smokers and nonsmokers were also analyzed.</p><p><strong>Results: </strong>UGT1A5 and 2B15 mRNAs were detected in human platelets. UGT1A5 expression was significantly higher in PRP than in liver, while it was about threefold lower. Both genes showed elevated expression in smokers' platelets, approximately 11.3-fold for UGT1A5 and 3.3-fold for UGT2B15, compared to nonsmokers.</p><p><strong>Conclusions: </strong>This study concludes the presence of UGT1A5 and 2B15 mRNA in human platelets and their elevated level in the platelets of smokers. Further research, including pharmacokinetic studies and protein-level validation, is needed to understand their functional significance.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2536306"},"PeriodicalIF":2.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144732933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deficiency of BLOS1 moderately impairs the biogenesis of platelet dense granules.","authors":"Yefeng Yuan, Wei Li","doi":"10.1080/09537104.2025.2545332","DOIUrl":"10.1080/09537104.2025.2545332","url":null,"abstract":"<p><p>Defects in platelet secretion contribute to hemorrhagic disorders and coagulopathies, primarily link to the biogenesis of lysosome-related organelles (LROs), namely alpha granules (AGs) and dense granules (DGs). While deficiencies in the biogenesis of lysosome-related organelles complex-1 (BLOC-1) are known to impair DG formation and platelet function, the distinct roles of individual BLOC-1 subunits remain unresolved. Here, we investigated BLOS1, a shared subunit of BLOC-1 and BLOC-1-related complex (BORC) encoded by <i>BLOC1S1</i>. Through comparative analysis of platelet-specific <i>Bloc1s1</i>-conditional knockout (<i>Bloc1s1-cKO</i>) mice and <i>sdy</i> mice (deficiency in BLOC-1 subunit dysbindin), we found that <i>Bloc1s1-cKO</i> platelets exhibited a 50% reduction in DG content compared to <i>sdy</i> mice, indicating BLOS1 deficiency causes moderate DG biogenesis defects. Consistently, agonist-induced DG secretion in <i>Bloc1s1-cKO</i> mice was moderately impaired relative to the severe defects in <i>sdy</i> mice. Distinct steady-state levels of granule proteins were observed between the two mutants. These findings suggest that dysbindin (only in BLOC-1) and BLOS1 (a shared BLOC-1 and BORC subunit) regulate LRO biogenesis and function in a different manner.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2545332"},"PeriodicalIF":2.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144874812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The renin-angiotensin system in healthy human platelets: expressed but inactive.","authors":"François Panosetti, François M Cuenot, Damian S Saint Auguste, Ana C Martins Cavaco, Allancer D C Nunes, Philip H J Lu, Céline Magrini, Max Molot, Gabriel Sanglard, Rodi Günçü, Yassine Zouaghi, Charles Béguelin, Augusto Martins Lima, Nikolaos Stergiopulos","doi":"10.1080/09537104.2025.2546982","DOIUrl":"10.1080/09537104.2025.2546982","url":null,"abstract":"<p><p>Platelets play a crucial role in arterial thrombus formation, offering potential for new antiplatelet therapies with reduced bleeding risk. Here, we investigated the role of the renin-angiotensin system (RAS) in human platelets and explored its potential link to COVID-19 coagulopathy. Experiments were performed <i>ex vivo</i> on healthy human platelets. The expression of RAS receptors (Mas, MrgD, ACE, ACE2, AT1 and AT2) was evaluated using western blot and immunofluorescence. Platelets were incubated <i>in vitro</i> with either Captopril or different RAS peptides including Alamandine, Angiotensin-I, Angiotensin-II, Angiotensin-(1-7), and Angiotensin-(1-9). Platelet adhesion was measured by spectrophotometry using BCECF fluorescence. Platelet activation and aggregation were analyzed using aggregometry after stimulation with extracellular matrix proteins. ACE and ACE2 activity were assessed using Fluorescent Peptides (FPS). We demonstrated that healthy human platelets express all the tested RAS receptors. However, RAS peptides did not modulate platelet adhesion or aggregation despite a wide range of concentrations tested. ACE activity was detected in platelet lysates, but it was not inhibited by Captopril, while ACE2 activity was undetectable. Our findings suggest that while RAS receptors are expressed in platelets, RAS peptides do not impact platelet function, at least in our experimental setting. COVID-19 coagulopathy may occur independently of the RAS.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2546982"},"PeriodicalIF":2.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144874844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From reticulated platelets to immature platelet fraction: structure, function, and clinical applications.","authors":"Yuxin Zhang, Ziyun Wang, Pan Zhou, Hongwei Zhang","doi":"10.1080/09537104.2025.2467383","DOIUrl":"10.1080/09537104.2025.2467383","url":null,"abstract":"<p><p>In comparison to mature platelets, reticulated platelets (RPs) are newly released from the bone marrow and exhibit a larger size, higher reactivity, and a greater quantity of RNA, and can be an agile indicator of platelet turnover. The transcriptome associated with platelet function is significantly upregulated in RPs, which is a possible explanation for RPs intrinsic hyper-reactivity. We presented a comprehensive overview of the detection techniques for RPs. Current methods to quantify RPs in clinical routine are flow cytometry and fully automated hematology analyzers (Sysmex-XE/XN, Abbott, ADVIA, Mindray), which make the detection of RPs simpler, faster and more affordable. The proportion of RPs increased in the circulation has potential diagnostic and prognostic values in multiple clinical settings (risk stratification in cardiovascular diseases, the effect on antiplatelet drugs, differential diagnosis of thrombocytopenia, monitor platelet recovery after bone marrow or stem cell transplantation, and other diseases). There have been several studies focusing on RPs in recent years, particularly in cardiovascular disease and thrombocytopenia. In this review we summarizes the current study with regard to RPs and discuss their likely contribution in clinical routine.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2467383"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143543018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Platelet-derived extracellular vesicles promote hair follicle growth through β-catenin signaling pathway.","authors":"Lei Wang, Yiwen Huang, Yajuan Wu, Yuanbo Huang, Zhou Lu, Panyu Wu, Shuo Meng, Tian Tian, Lei Cao","doi":"10.1080/09537104.2025.2498353","DOIUrl":"https://doi.org/10.1080/09537104.2025.2498353","url":null,"abstract":"<p><p>The application of platelet concentrates such as platelet-rich plasma (PRP) for the treatment of hair loss is impeded by the absence of standardized preparation protocols and storage conditions. Providing off-the-shelf controlled product methods and inheriting regenerative function of platelets, platelet-derived extracellular vesicles (PEVs) can be a promising alternative to surpass platelet concentrates limitations. This study aimed to investigate the effects of PEVs on cultured dermal papilla cells (DPCs) and hair follicles (HFs) in animal model. PEVs were prepared from fresh apheresis platelets and characterized. Their impact on the proliferation and migration of DPCs was explored. After subcutaneous administration of PEVs in a mouse model of depilation-induced hair regeneration, we observed the accelerated transition of HFs from the telogen to the anagen phase, and found the β-catenin signaling pathway was involved. These results indicate that PEVs activate DPCs and promote HF growth effectively. The PEVs from apheresis platelets offer a robust alternative for the treatment of hair loss.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2498353"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143977013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dornhorst's model revisited: an error identified in the equation for platelet survival.","authors":"Woo Young Shin, Kyeong Deok Kim, Keon-Young Lee","doi":"10.1080/09537104.2025.2547926","DOIUrl":"https://doi.org/10.1080/09537104.2025.2547926","url":null,"abstract":"","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2547926"},"PeriodicalIF":2.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145131771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of testosterone on platelet activation and inflammation in transgender men.","authors":"Lieve Mees van Zijverden, Moya Henriëtte Schutte, Marieke Tebbens, Milou Cecilia Madsen, Jeske Joanna Katarina van Diemen, Chantal Maria Wiepjes, Martin den Heijer, Abel Thijs","doi":"10.1080/09537104.2025.2567294","DOIUrl":"https://doi.org/10.1080/09537104.2025.2567294","url":null,"abstract":"<p><strong>Background and aims: </strong>Transgender men (female sex assigned at birth, male gender identity) who use testosterone have a higher cardiovascular risk compared to women and men from the general population, which cannot be fully attributed to traditional cardiovascular risk factors. Platelet activation and (endothelial) inflammation are interconnected mechanisms in the process of primary hemostasis, and thus the development of cardiovascular disease, but the impact of testosterone on these mechanisms is largely unexplored. Hence, we aimed to investigate the effect of testosterone on platelet activation and inflammation in vivo.</p><p><strong>Methods: </strong>In this prospective cohort study 18 transgender men were included. Blood samples were taken at baseline and at 6, 12 and 52 weeks after testosterone initiation. We measured seven platelet activation markers (plasma thromboxane B2, Closure Time measured in two ways, CD63, CD62p, platelet-leukocyte complexes, immature platelet fraction), and twelve inflammation markers (high sensitivity CRP and 11 cytokines). Percentage changes relative to baseline were calculated at each time point using linear mixed model analyses.</p><p><strong>Results: </strong>Platelet activation markers CD63, CD62p, and platelet-leukocyte complexes exhibited an initial tendency to increase at week 6, then slightly decreased at week 12, and again increased at week 52. Closure Time and immature platelet fraction remained stable throughout the study period. The collective of inflammation markers exhibited an overall tendency toward increase throughout the study period, which was most pronounced at week 52.</p><p><strong>Conclusion: </strong>The results suggest that testosterone administration may increase platelet activation and inflammation. This may contribute to the higher cardiovascular risk in transgender men.</p><p><strong>Study registration: </strong>EudraCT #2017-003072-31.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2567294"},"PeriodicalIF":2.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of in-hospital net clinical outcomes of ticagrelor and clopidogrel in acute coronary syndrome patients stratified by CRUSADE score: findings from the CCC-ACS registry.","authors":"Zuoyi Zhou, Haotai Xie, Fangfang Fan, Fan Yang, Jie Jiang, Bo Zheng, Yan Zhang, Yongchen Hao, Jing Liu, Yanjun Gong, Dong Zhao, Sidney C Smith, Yong Huo","doi":"10.1080/09537104.2025.2570743","DOIUrl":"10.1080/09537104.2025.2570743","url":null,"abstract":"<p><strong>Objectives: </strong>To compare the effect of ticagrelor and clopidogrel on net clinical outcomes in patients with acute coronary syndrome (ACS) and assess the CRUSADE score's utility in guiding the selection of P2Y12 inhibitors.</p><p><strong>Design: </strong>Nationwide observational cohort study using data from the CCC-ACS registry.</p><p><strong>Setting: </strong>About 159 tertiary hospitals and 82 secondary hospitals across China.</p><p><strong>Participants: </strong>About 70,319 patients with ACS who were prescribed dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor within 24 h of the first medical contact. Inclusion criteria were based on ACS diagnosis, and exclusion criteria included coronary artery bypass grafting, thrombolysis, use of oral anticoagulants, atrial fibrillation, or incomplete data.</p><p><strong>Main outcome measures: </strong>Primary endpoint was in-hospital net adverse clinical events (NACE) defined as the composite of all-cause mortality, major ischemic events (recurrent myocardial infarction, stent thrombosis, ischemic stroke), and major bleeding (BARC types 3b, 3c, 5). Secondary endpoints included all-cause mortality, major ischemic events, major bleeding, intracranial bleeding, and major adverse cardiovascular events (MACE).</p><p><strong>Results: </strong>After propensity score matching, no significant difference was found in NACE (1.6% in both groups; OR 0.97, 95% CI 0.82 to 1.16, <i>p</i> = .74) or all-cause mortality (0.7% in both groups; OR 0.92, 95% CI 0.71 to 1.20, <i>p</i> = .55) between ticagrelor and clopidogrel. However, ticagrelor was associated with significantly lower risks of MACE (1.0% vs. 1.2%; OR 0.80, 95% CI 0.65 to 0.99, <i>p</i> = .04) and major ischemic events (0.4% vs. 0.5%; OR 0.70, 95% CI 0.51 to 0.96, <i>p</i> = .03), but higher risks of major bleeding (1.6% vs. 1.1%; OR 1.50, 95% CI 1.24 to 1.81, <i>p</i> < .001), intracranial bleeding (0.3% vs. 0.1%; OR 2.24, 95% CI 1.35 to 3.72, <i>p</i> = .002), and gastrointestinal bleeding (0.9% vs. 0.5%; OR 1.74, 95% CI 1.33 to 2.28, <i>p</i> < .001). The CRUSADE score significantly interacted with the impact of P2Y12 inhibitor choice on clinical outcomes. In those with a CRUSADE score >40, ticagrelor was linked to higher risks of NACE (<i>p</i> = .03) and all-cause mortality (<i>p</i> = .04), while lower CRUSADE scores (<30) favored the use of ticagrelor.</p><p><strong>Conclusions: </strong>In this observational study of in-hospital outcomes, ticagrelor was associated with reduced ischemic events but increased bleeding risks compared to clopidogrel in ACS patients. The CRUSADE score could be used to identify patients who may benefit from either clopidogrel or ticagrelor. Personalized treatment strategies using clinical risk scores may help optimize outcomes and minimize bleeding complications in ACS management.</p><p><strong>Trial registration: </strong>ClinicalTrials.gov (NCT02306616).</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2570743"},"PeriodicalIF":2.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145378491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thiazole orange: a complement to established methods for diagnosing inherited dense granule defects.","authors":"Myriam Martin, Karin Strandberg, Eva Zetterberg, Eva Norström","doi":"10.1080/09537104.2025.2592683","DOIUrl":"https://doi.org/10.1080/09537104.2025.2592683","url":null,"abstract":"<p><p>Inherited delta storage pool deficiencies are likely underdiagnosed due to limitations in available diagnostic tools. Achieving accurate diagnosis is thus challenging for clinical laboratories highlighting the need for improved methods. Our aim was to explore thiazole orange (TO) as a flow cytometric marker for dense granules and compare it with mepacrine, reported to have low positive predictive value, after optimization of both protocols. TO, typically used for reticulocyte marking, binds dense granules at high concentrations producing a strong signal in resting platelets. Upon activation, the signal substantially decreased due to degranulation, which was less pronounced for mepacrine. Gradual dense granule release could only be followed with TO indicating that solely TO can distinguish quantitative defects from release defects. In a small pilot study TO staining was compared to light aggregometry and flow cytometric CD63 exposure in patients with suspected inherited platelet disorders. Of 15 samples, five showed abnormal TO results; in three, the other methods agreed with granule defects, but solely TO differentiates quantitative defects from release defects. Of note, two samples showed slightly decreased TO staining, despite normal aggregometry and CD63 exposure. TO is a promising diagnostic tool for dense granule defects and may be a valuable complement in the diagnostic workup for inherited platelet disorders.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2592683"},"PeriodicalIF":2.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145649166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiometabolic risk factor burden associates with an immature platelet profile.","authors":"Carine E Hamo, Matthew Muller, Emily Rosenfeld, Yuhe Xia, Adedoyin Akinlonu, Elliot Luttrell-Williams, Tessa J Barrett, Jeffrey S Berger","doi":"10.1080/09537104.2025.2459800","DOIUrl":"10.1080/09537104.2025.2459800","url":null,"abstract":"<p><p>Cardiometabolic risk factors, obesity, diabetes and hyperlipidemia contribute to cardiovascular disease (CVD). While platelets are involved in CVD pathogenesis, the relationship between risk factor burden on platelet indices and the platelet transcriptome remains uncertain. Blood was collected from CVD-free adults, measuring platelet count, mean platelet volume (MPV), immature platelet fraction (IPF), and absolute immature platelet fraction (AIPF) by hemogram. Platelets were isolated and analyzed via RNA sequencing. Participants were stratified by number of cardiometabolic risk factors (diabetes, obesity, hyperlipidemia). We calculated median (IQR) values of platelet indices and p-for-trend via linear regression across risk factor burden. To evaluate the association between risk factor burden and platelet transcripts, we performed multivariable linear regression adjusting for age, sex, and race/ethnicity. Among 141 participants, (50.5 ± 14.8 years, 42% male, 26% Black) risk factor burden was associated with increasing platelet size, IPF, and AIPF but not platelet count. Platelet RNA sequencing identified 100 differentially expressed transcripts (<i>p</i> < .01; 66 upregulated, 34 downregulated). Gene ontology enrichment analysis demonstrated upregulated pathways of secondary metabolic processes (NES = 1.96, <i>p</i> < .01), and hematopoietic stem cell proliferation (NES = 1.95, <i>p</i> < .01). Greater cardiometabolic risk factor burden is associated with increased platelet size and immaturity and suggesting novel platelet-mediated mechanisms linking risk factor burden with CVD.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2459800"},"PeriodicalIF":3.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11801799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143067532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}