Platelets最新文献

{"title":"Platelets induce VISTA expression and modulate the ovarian tumor microenvironment.","authors":"Hani Lee, Brianne Sager, Anil Sood, Vahid Afshar-Kharghan, Min Soon Cho","doi":"10.1080/09537104.2026.2644366","DOIUrl":"10.1080/09537104.2026.2644366","url":null,"abstract":"<p><p>Immune checkpoint regulators, such as the V-domain Ig suppressor of T cell activation (VISTA), play a critical role in shaping the tumor microenvironment (TME) and facilitating immune evasion. In ovarian cancer, VISTA exhibits more abundant and consistent expression than other immune checkpoints, including Programmed Death-Ligand 1 (PD-L1). This study examined the role of platelets in the regulation of VISTA in ovarian cancer using both in vitro and in vivo models. Our findings demonstrate that platelets upregulate VISTA expression in both myeloid and tumor cells, thereby promoting an immunosuppressive TME. Elevated VISTA levels were associated with higher platelet counts and poorer clinical outcomes. These results highlight that platelet-mediated VISTA upregulation is a potential therapeutic target for improving antitumor immune responses in ovarian cancer.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2644366"},"PeriodicalIF":2.6,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147499595","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":"GPVI deficiency reduces clot size and murine thrombosis in normoglycaemic but not hyperglycemic conditions.","authors":"Julia S Gauer, Cédric Duval, Helen R McPherson, Amanda D V MacCannell, Lee D Roberts, Khalid M Naseem, Ramzi A Ajjan, Robert A S Ariëns","doi":"10.1080/09537104.2026.2646681","DOIUrl":"https://doi.org/10.1080/09537104.2026.2646681","url":null,"abstract":"<p><strong>Background: </strong>Glycoprotein (GP)VI is involved in platelet activation, procoagulant phenotype development and reactive oxygen species (ROS) production. Patients with diabetes have altered platelet reactivity and abnormal clot structure, contributing to elevated thrombosis risk. The role of GPVI in clot formation in hyperglycemia is under-investigated.</p><p><strong>Objectives: </strong>To compare the effect of GPVI-deficiency on ROS production and ex vivo and in vivo clot formation in normo- vs hyperglycemic mice.</p><p><strong>Methods: </strong>Wild-type (WT) and GPVI-deficient (GPVI^-/-) mice had access to hyperglycemic (30% sucrose) or normoglycaemic (standard) diet for 8-weeks. ROS and mitochondrial activity (CS) were measured in isolated platelets. Clot contraction was performed with whole blood. Thrombus formation in vivo was assessed by inferior vena cava (IVC) ligation.</p><p><strong>Results: </strong>Hyperglycemia increased ROS and CS activity in WT but not GPVI^-/- mice. Clot weight was decreased in GPVI^-/- vs WT mice in normoglycaemia, but these effects were lost in hyperglycemia. Clot weight after IVC ligation was reduced in GPVI^-/- vs WT mice in normoglycaemia, with the inverse observed in hyperglycemia.</p><p><strong>Conclusions: </strong>Our data suggest that clot formation is affected differentially by absence of GPVI in normo- vs hyperglycemia, supporting a role for GPVI in thrombosis under normoglycaemic conditions only.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2646681"},"PeriodicalIF":2.6,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147499468","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":"Pilot study on cannabis-induced alterations in platelet function: implications for transfusion medicine.","authors":"Geneviève Laflamme, Hind Hamzeh-Cognasse, Fabrice Cognasse, Lionel Loubaki","doi":"10.1080/09537104.2026.2644368","DOIUrl":"https://doi.org/10.1080/09537104.2026.2644368","url":null,"abstract":"<p><p>Platelet transfusions are essential in the management of thrombocytopenia, bleeding disorders, and hematologic malignancies. With cannabis use rising worldwide, its impact on donor platelet quality and transfusion efficacy remains poorly understood. This study investigated the effects of cannabis joint extracts (CJE) on platelet activation, pro-coagulant phenotype, mitochondrial function, and cytokine/chemokine release, with implications for transfusion safety. Human platelets were exposed in vitro to increasing concentrations of two CJE with distinct cannabinoid profiles: Orchid (O-CJE, THC 10.4%, CBD 14.7%) and QCGold (G-CJE, THC 25.5%, CBD 0.04%). Platelet activation (CD62P, Annexin V), mitochondrial depolarization, ATP levels, aggregation responses, and cytokine secretion (CCL3, PF4) were assessed. RBC lysate experiments were performed to assess the role of hemolysis. The involvement of CB1 and CB2 receptors was tested using specific antagonists, and activation of p38 MAPK and NF-κB pathways was evaluated. Functional effects of platelet supernatants were examined on EA.hy926 endothelial cells. CJE exposure induced dose-dependent platelet activation, characterized by increased CD62P expression, Annexin V binding, mitochondrial depolarization, and ATP depletion, consistent with metabolic stress. Platelet aggregation in response to ADP, collagen, and arachidonic acid was impaired, suggesting a pre-activated or refractory phenotype. RBC lysate did not reproduce the observed effects, indicating hemolysis is unlikely to be the underlying mechanism. CBR1 and CBR2 antagonists did not attenuate platelet activation, while signaling analysis revealed activation of p38 MAPK and NF-κB pathways. Exploratory proteomics indicated modulation of proteins involved in angiogenesis, cytoskeletal organization, and stress responses. Elevated plasma levels of CCL3 and PF4 and endothelial activation (IL-6 secretion, CD54, CD62P, CD62E expression) further suggested a pro-inflammatory environment. Cannabis exposure can alter platelet phenotype and signaling under in vitro conditions, potentially affecting platelet function and interactions with the vascular endothelium. However, these findings require confirmation in vivo to determine their clinical relevance. Future studies should aim to establish exposure thresholds and clarify whether cannabis use has implications for transfusion safety, given potential risks of reduced efficacy or increased thrombotic complications in recipients.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2644368"},"PeriodicalIF":2.6,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147499491","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-rich plasma concentrations regulate MSCs osteogenesis via MAPK/PI3K-AKT pathways to mitigate inflammatory bone loss.","authors":"Shaochuan Wang, Debin Guo, Shidan Li, Ruohui Tang, Hao Jiang, Xiaoming Li, Youbin Li, Jing Yang, Lei Li, Jun Fei","doi":"10.1080/09537104.2026.2642053","DOIUrl":"https://doi.org/10.1080/09537104.2026.2642053","url":null,"abstract":"<p><p>Bone maintains a dynamic and stable state through the orchestration of osteoclasts and osteoblasts. Osteoblasts are derived mainly from mesenchymal stem cell (MSC) and are responsible for bone formation. The inhibition of osteoblast proliferation and differentiation is involved in many diseases, including osteoporosis, osteoarthritis, infected bone defects, and inflammatory aseptic loosening of implants. Given the currently limited treatment options, exploring new methods to promote bone formation is an important focus significant for orthopedists. Platelet-rich plasma (PRP), an autologous substance that is rich in various growth factors, is widely used in regenerative medicine. However, the effect of PRP on inflammatory bone destruction remains unclear. We investigated the effects of PRP on the viability of MSC, and the impact of different concentrations of PRP (1% and 3%, respectively) on cell death, proliferation, and differentiation. Furthermore, we tested the therapeutic effect of different concentrations of PRP (1% and 3%) on LPS-induced inflammatory bone destruction in vivo. PRP enhanced the cellular activity of MSC and promoted osteogenesis. A higher concentration of PRP (3%) primarily reduced the death and increased the proliferation of in LPS-treated MSC via the PI3K/AKT pathway, while a lower concentration of PRP (1%) promoted MSC differentiation into osteoblasts through the MAPK pathway. Consistent with in vitro experiments, we validated the protective effect of PRP against LPS-induced bone loss by increasing bone formation in vivo. These results suggest that different concentrations of PRP can ameliorate LPS-induced inflammatory bone loss through distinct mechanisms.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2642053"},"PeriodicalIF":2.6,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147623572","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 use of light transmission aggregometry for monitoring platelet transfusion response in a small case cohort of Glanzmann thrombasthenia patients: a hypothesis-generating study.","authors":"Karlijn H G Rutten, Olga Tsiamita, Sean Platton, Mathieu Fiore, Rolf T Urbanus, Suthesh Sivapalaratnam, Roger E G Schutgens","doi":"10.1080/09537104.2026.2621761","DOIUrl":"https://doi.org/10.1080/09537104.2026.2621761","url":null,"abstract":"<p><p>Light transmission aggregometry (LTA) is commonly used to diagnose platelet disorders and has a specific pattern in Glanzmann thrombasthenia (GT). As there is currently no adequate test to assess the efficacy of platelet transfusion, we explored whether LTA can be used to monitor the platelet response following platelet transfusion. We retrospectively evaluated LTA results after platelet transfusion in four patients with GT. After transfusion of two units of platelets, aggregation assessed by LTA remained reduced for all platelet agonists except ristocetin, despite a satisfactory clinical effect on hemostasis. One patient received seven units, after which a change in LTA results was observed. In this heterogeneous case cohort, the LTA response did not correlate with the clinical response after platelet transfusion in GT. To draw definitive conclusions, a study in a larger population that controls for influencing factors - such as the timing and dose of platelet transfusion and the use of a standardized LTA procedure - should be conducted.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2621761"},"PeriodicalIF":2.6,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146087053","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":"Neural network reveals platelet age from fluorescence microscopy images.","authors":"Johan A Slotman, Maurice Swinkels, Sophie Hordijk, Daan Te Rietmole, Bart Geverts, Petra E Bürgisser, Joyce Bestebroer, Ihor Smal, Thomas R L Klei, Adriaan B Houtsmuller, Frank W G Leebeek, Ruben Bierings, A J Gerard Jansen","doi":"10.1080/09537104.2026.2656268","DOIUrl":"https://doi.org/10.1080/09537104.2026.2656268","url":null,"abstract":"<p><p>Platelets are small, anucleate cells with a primary physiological role in vascular damage repair (hemostasis) and initiation of thrombus formation in response to vascular injury. Platelets circulate approximately 7-10 days, slowly undergoing age-related changes in molecular composition, morphology, activation capacity, function, and surface receptor density. As older platelets are associated with poor clinical outcome, no <i>in vitro</i> tests are available to predict platelet age, or to determine the fitness of platelet transfusion products. In this study, we developed a convolutional neural network model that could determine platelets' chronological age from confocal microscopic images. The model was trained using platelets stored in platelet-rich plasma up to 8 hours and using routine platelet concentrates up to 10 days. The model predicted chronological age of stored platelets with >97% accuracy. To test our model <i>in vivo</i>, we analyzed a cohort of patients with acute myeloid leukemia, experiencing thrombocytopenia due to chemotherapy. Our model could reliably distinguish <i>in vivo</i> between samples with younger and older platelets during the course of treatment. This study demonstrates the ability to predict platelets' chronological age both <i>in vitro during storage</i> and <i>in vivo</i>, which may impact clinical transfusion medicine and the diagnosis and treatment of patients with platelet disorders.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2656268"},"PeriodicalIF":2.6,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147699604","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":"Immune thrombocytopenia triggered by dostarlimab in a patient with endometrial carcinoma: first reported case.","authors":"Adolfo Fernández-Sánchez, Pablo García-Jaén, Carlos Puerta-Vázquez, M Belén Pazmiño-Zambrano, Pablo Reguera-Puertas, José Ramón González-Porras, José María Bastida","doi":"10.1080/09537104.2025.2601056","DOIUrl":"10.1080/09537104.2025.2601056","url":null,"abstract":"<p><p>Immune checkpoint inhibitors (ICIs) have transformed the treatment landscape for various malignancies, but they are associated with a range of immunerelated adverse events, including rare hematological complications. Immune thrombocytopenia (ITP) has been reported with other antiPD1 agents such as nivolumab and pembrolizumab, but to date, no cases have been described with dostarlimab. We report the first case of ITP in a patient receiving dostarlimab for relapsed endometrial carcinoma. A 55yearold woman developed severe thrombocytopenia (3 × 10⁹/L) accompanied by rectal bleeding, resulting in a lifethreatening condition. Secondary causes were excluded, and bone marrow findings supported a diagnosis of ITP. Initial treatment with highdose corticosteroids and intravenous immunoglobulin achieved only a partial response, while sustained platelet recovery was obtained with the addition of romiplostim. The patient remained on dostarlimab following hematological recovery without further episodes of ITP. This case highlights a potentially lifethreatening adverse effect of a widely used immunotherapy and underscores the importance of early recognition and timely escalation of treatment in ICIinduced ITP.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2601056"},"PeriodicalIF":2.6,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145810905","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":"Sixty years of research into ancestry differences in platelet function.","authors":"Jillian Teichman, Andrew D Johnson","doi":"10.1080/09537104.2026.2649282","DOIUrl":"10.1080/09537104.2026.2649282","url":null,"abstract":"<p><p>Studies investigating the role of differential platelet function across various ancestry groups have been ongoing since at least the middle twentieth century. Consistently identified trends include differential frequency of CD36 deficiencies, variability in the efficacy of the antiplatelet functions of clopidogrel, increased PAR4 reactivity observed among African ancestry individuals, and reduced ristocetin-induced platelet aggregation also observed in African ancestry. Nonetheless, consensus is lacking in many areas. Replication in many of these studies is poor, utilized models may lack the necessary covariates to effectively capture environmental effects, and the represented cohorts disproportionately lean North American. Further comparative research of platelet phenotypes may yield important clinical insights and benefits; though to accomplish this a collaborative, international effort between institutes would be required. In this review, we discuss what is currently understood regarding differential platelet reactivity between ancestry groups, what areas are inadequately characterized, and the technical and organizational aspects which should be considered in future research.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2649282"},"PeriodicalIF":2.6,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13118511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147628396","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}

{"title":"Single-cell transcriptome deciphers key targets of thrombopoietin receptor agonists and immune microenvironment characteristics of immune thrombocytopenia.","authors":"Wanru Wang, Haoxu Wang, Xiaohan Wan, Junying Cao, Ruixue Wang, Ming Hou","doi":"10.1080/09537104.2026.2651849","DOIUrl":"https://doi.org/10.1080/09537104.2026.2651849","url":null,"abstract":"<p><p>Thrombopoietin receptor agonists (TPO-RAs) represent a cornerstone in immune thrombocytopenia (ITP) management, yet their molecular mechanisms remain incompletely elucidated. This study systematically deciphered the key targets and signaling networks of four TPO-RAs (romiplostim, eltrombopag, avatrombopag, hetrombopag) in ITP pathogenesis. Network pharmacology was integrated with single-cell high-dimensional weighted gene co-expression network analysis (hdWGCNA) using bone marrow scRNA-seq data from ITP patients and healthy controls. Metacell-based co-expression modules to hematopoietic bone marrow cells were identified. Drug targets were curated from multiple databases, and candidate genes were screened by intersecting differentially expressed genes (DEGs), cell specific modules, and TPO-RA targets. Molecular docking, pseudotime trajectory analysis, and in silico gene knockdown were employed for functional validation. Intersection analysis revealed five key genes (CACNA1A, CSF1R, PKN1, CD9, DSTYK). Molecular docking demonstrated strong binding affinities between TPO-RAs and key targets. The ITP bone marrow niche exhibited rewired cell-cell communication, with enhanced T cell-initiated signaling and aberrant megakaryocyte-T cell interactions. Pseudotime analysis uncovered disrupted megakaryocyte maturation dynamics. In silico knockdown revealed CACNA1A, CSF1R, and PKN1 dysregulation exacerbated neutrophil hyperactivity, while CD9 and DSTYK knockdown impaired mitotic regulation. This study delineated mechanisms of TPO-RAs, highlighting five key genes that orchestrate dysregulated thrombopoiesis and immune dysfunction in ITP. The integration of in silico strategies identified novel targets for optimizing ITP therapy.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2651849"},"PeriodicalIF":2.6,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147593941","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":"Bridging specialties: repurposing platelet drugs prescribed by cardiologists to help infectious disease doctors treat <i>Staphylococcus aureus</i> bacteremia.","authors":"Matthew Geriak, Dani Geriak, Victor Nizet, George Sakoulas","doi":"10.1080/09537104.2025.2612045","DOIUrl":"10.1080/09537104.2025.2612045","url":null,"abstract":"<p><p>The platelet is the most important cell in the bloodstream in providing endovascular immunity against <i>Staphylococcus aureus</i> bacteremia. Both quantitative and qualitative thrombocytopenia have been associated with increased mortality in patients with <i>S. aureus</i> bacteremia. Patients with end-stage renal disease are particularly vulnerable to both an increased risk of getting <i>S. aureus</i> bacteremia and endocarditis, but also in treatment failure resulting in prolonged infection and relapse. In this commentary, we highlight the important host-pathogen relationship between <i>S. aureus</i> and the human platelet. In particular, we describe virulence factor-mediated platelet clearance from the circulation and improvement in platelet counts as a marker of treatment success. P2Y12 inhibitors deployed in the treatment of cardiovascular disease have been shown to attenuate the effect of <i>S. aureus</i> on platelet clearance. Therefore, we believe that partnerships between investigators in cardiology, hematology, and infectious disease with particular focus on platelet pathophysiology are poised to improve outcomes in select patients with <i>S. aureus</i> endovascular infection.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2612045"},"PeriodicalIF":2.6,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145990347","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}