ArticleBlood2016
CCL5 derived from platelets increases megakaryocyte proplatelet formation.
Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
66 citing papers in PubMed, 119 citations in OpenAlex.
- CCL5 exposure promotes acute and transient megakaryopoiesis and hematopoietic progenitor expansion.Stem cell reports · 2026Article
- A systems herbal-to-molecule and transcriptomic strategy identifies emodin as an ESR1-targeting phytochemical driving thrombopoiesis.Chinese medicine · 2026Article
- Platelet-neutrophil cooperation in cancer: mechanisms of metastatic niche formation and implications for prognostic stratification and therapy.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Exosomal Protein Biomarkers for Predicting Early Neurological Deterioration Following Intravenous Thrombolysis in Acute Ischemic Stroke.Translational stroke research · 2026Article
- Engineering platelets as cancer therapeutics.Nature reviews. Clinical oncology · 2026Review
- Induction of moderate DNA damage enhances megakaryopoiesis and platelet production.Blood advances · 2026Article
- Thrombocytosis in cancer patients: when more is not better-in fact, the opposite.Cancer metastasis reviews · 2026Review
- `Inflammatory mediators differentially regulate megakaryopoiesis and thrombopoiesis in myelofibrosis and essential thrombocythemia.Scientific reports · 2025Article
- Beyond Thrombopoiesis: The Immune Functions of Megakaryocytes in Bacterial Infections and Sepsis.International journal of molecular sciences · 2025Review
- Production of plateletsHaematologica · 2025Article
- An unconquered challenge in MDS: review of pathophysiology, clinical manifestations, and management options of MDS with thrombocytopenia.Annals of hematology · 2025Review
- Neutrophils and Platelets as Key Players in the Pathogenesis of ANCA-Associated Vasculitis and Potential Sources of Disease Activity Biomarkers.Diagnostics (Basel, Switzerland) · 2025Review
- Article
- Harnessing immunotherapeutic molecules and diagnostic biomarkers as human-derived adjuvants for MERS-CoV vaccine development.Frontiers in immunology · 2025Review
- The CCL5/CCR5/SHP2 axis sustains Stat1 phosphorylation and activates NF-κB signaling promoting M1 macrophage polarization and exacerbating chronic prostatic inflammation.Cell communication and signaling : CCS · 2024Article
- Thrombocytopenia in dengue infection: mechanisms and a potential application.Expert reviews in molecular medicine · 2024Review
- SARS-CoV-2 infection modifies the transcriptome of the megakaryocytes in the bone marrow.Blood advances · 2024Article
- Low platelet count at diagnosis of anti-neutrophil cytoplasmic antibody-associated vasculitis is correlated with the severity of disease and renal prognosis.Clinical and experimental medicine · 2024Article
- Article
- A let-7 microRNA-RALB axis links the immune properties of iPSC-derived megakaryocytes with platelet producibility.Nature communications · 2024Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
In times of physiological stress, platelet count can transiently rise. What initiates this reactive thrombocytosis is poorly understood. Intriguingly, we found that treating megakaryocytes (MKs) with the releasate from activated platelets increased proplatelet production by 47%. Platelets store inflammatory cytokines, including the chemokine ligand 5 (CCL5, RANTES); after TRAP activation, platelets release over 25 ng/mL CCL5. We hypothesized that CCL5 could regulate platelet production by binding to its receptor, CCR5, on MKs. Maraviroc (CCR5 antagonist) or CCL5 immunodepletion diminished 95% and 70% of the effect of platelet releasate, respectively, suggesting CCL5 derived from platelets is sufficient to drive increased platelet production through MK CCR5. MKs cultured with recombinant CCL5 increased proplatelet production by 50% and had significantly higher ploidy. Pretreating the MK cultures with maraviroc prior to exposure to CCL5 reversed the augmented proplatelet formation and ploidy, suggesting that CCL5 increases MK ploidy and proplatelet formation in a CCR5-dependent manner. Interrogation of the Akt signaling pathway suggested that CCL5/CCR5 may influence proplatelet production by suppressing apoptosis. In an in vivo murine acute colitis model, platelet count significantly correlated with inflammation whereas maraviroc treatment abolished this correlation. We propose that CCL5 signaling through CCR5 may increase platelet counts during physiological stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.