ArticleThe Journal of experimental medicine1998
Transendothelial migration of megakaryocytes in response to stromal cell-derived factor 1 (SDF-1) enhances platelet formation.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
68 citing papers in PubMed, 245 citations in OpenAlex.
- Chemotherapy-induced thrombocytopenia: from "platelet counting" to ecological repair of the bone marrow.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026Review
- Phenotyping and clinical utility of phagocytic polyploid giant cancer macrophages in blood.Cancer letters · 2025Article
- Article
- Production of plateletsHaematologica · 2025Article
- The role of immune cells settled in the bone marrow on adult hematopoietic stem cells.Cellular and molecular life sciences : CMLS · 2024Review
- Pim Kinase Inhibition Disrupts CXCR4 Signalling in Megakaryocytes and Platelets by Reducing Receptor Availability at the Surface.International journal of molecular sciences · 2024Article
- Actin-bundling protein L-plastin promotes megakaryocyte rigidity and dampens proplatelet formation.Haematologica · 2024Article
- Megakaryocytes respond during sepsis and display innate immune cell behaviors.Frontiers in immunology · 2023Article
- CXCR4eLife · 2022Article
- JAK2V617F Mutant Megakaryocytes Contribute to Hematopoietic Aging in a Murine Model of Myeloproliferative Neoplasm.Stem cells (Dayton, Ohio) · 2022Article
- The bone marrow niche from the inside out: how megakaryocytes are shaped by and shape hematopoiesis.Blood · 2022Review
- Review
- Megakaryocytes as the Regulator of the Hematopoietic Vascular Niche.Frontiers in oncology · 2022Review
- Megakaryocyte Diversity in Ontogeny, Functions and Cell-Cell Interactions.Frontiers in oncology · 2022Article
- Lung megakaryocytes display distinct transcriptional and phenotypic properties.Blood advances · 2020Article
- miR-125a-5p regulates megakaryocyte proplatelet formation via the actin-bundling protein L-plastin.Blood · 2020Article
- Article
- Presence of intra-tumoral CD61+ megakaryocytes predicts poor prognosis in non-small cell lung cancer.Translational lung cancer research · 2019Article
- New Insights Into the Differentiation of Megakaryocytes From Hematopoietic Progenitors.Arteriosclerosis, thrombosis, and vascular biology · 2019Review
- Megakaryocytes as immune cells.Journal of leukocyte biology · 2019Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Although thrombopoietin has been shown to promote megakaryocyte (MK) proliferation and maturation, the exact mechanism and site of platelet formation are not well defined. Studies have shown that MKs may transmigrate through bone marrow endothelial cells (BMEC), and release platelets within the sinusoidal space or lung capillaries. In search for chemotactic factor(s) that may mediate transmigration of MKs, we have discovered that mature polyploid MKs express the G protein-coupled chemokine receptor CXCR4 (Fusin, LESTR). Therefore, we explored the possibility that stromal cell-derived factor 1 (SDF-1), the ligand for CXCR4, may also induce transendothelial migration of mature MKs. SDF-1, but not other CXC or CC chemokines, was able to mediate MK migration (ED50 = 125 pmol/liter). The MK chemotaxis induced by SDF-1 was inhibited by the CXCR4-specific mAb (12G5) and by pertussis toxin, demonstrating that signaling via the G protein-coupled receptor CXCR4 was necessary for migration. SDF-1 also induced MKs to migrate through confluent monolayers of BMEC by increasing the affinity of MKs for BMEC. Activation of BMEC with interleukin 1beta resulted in a threefold increase in the migration of MKs in response to SDF-1. Neutralizing mAb to the endothelial-specific adhesion molecule E-selectin blocked the migration of MKs by 50%, suggesting that cellular interaction of MKs with BMEC is critical for the migration of MKs. Light microscopy and ploidy determination of transmigrated MKs demonstrated predominance of polyploid MKs. Virtually all platelets generated in the lower chamber also expressed CXCR4. Platelets formed in the lower chamber were functional and expressed P-selectin (CD62P) in response to thrombin stimulation. Electron microscopy of the cells that transmigrated through the BMEC monolayers in response to SDF-1 demonstrated the presence of intact polyploid MKs as well as MKs in the process of platelet formation. These results suggest that SDF-1 is a potent chemotactic factor for mature MKs. Expression of CXCR4 may be the critical cellular signal for transmigration of MKs and platelet formation.
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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.