ArticleThe American journal of pathology2008
Bone morphogenetic proteins are overexpressed in the bone marrow of primary myelofibrosis and are apparently induced by fibrogenic cytokines.
Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 85 citations in OpenAlex.
- What Explains the Pattern of Fibrosis in Chronic Graft-Versus-Host Disease?Clinical transplantation · 2026Review
- Inflammatory and Immune Microenvironment in Myeloproliferative Neoplasms: Pathogenic Mechanisms and Therapeutic Opportunities.Cancers · 2026Review
- Transcriptomic comparison of bone marrow CD34 + cells and peripheral blood neutrophils from ET patients with JAK2 or CALR mutations.BMC genomic data · 2023Article
- Megakaryocyte Secreted Factors Regulate Bone Marrow Niche Cells During Skeletal Homeostasis, Aging, and Disease.Calcified tissue international · 2023Review
- Essential thrombocythaemia progression to the fibrotic phase is associated with a decrease in JAK2 and PDL1 levels.Annals of hematology · 2022Article
- Carbohydrates and ginsenosides in shenmai injection jointly improve hematopoietic function during chemotherapy-induced myelosuppression in mice.Chinese medicine · 2022Article
- The immune landscape in BCR-ABL negative myeloproliferative neoplasms: inflammation, infections and opportunities for immunotherapy.British journal of haematology · 2022Review
- Momelotinib: an emerging treatment for myelofibrosis patients with anemia.Journal of hematology & oncology · 2022Review
- Primary Immune Thrombocytopenia and Essential Thrombocythemia: So Different and yet Somehow Similar-Cases Series and a Review of the Literature.International journal of molecular sciences · 2021Review
- NK Cells in Myeloproliferative Neoplasms (MPN).Cancers · 2021Review
- A Broad Overview of Signaling inCancers · 2021Review
- Immunotherapy in Myeloproliferative Diseases.Cells · 2020Review
- Incremental Utility of Right Ventricular Dysfunction in Patients With Myeloproliferative Neoplasm-Associated Pulmonary Hypertension.Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography · 2019Article
- The Rationale for Immunotherapy in Myeloproliferative Neoplasms.Current hematologic malignancy reports · 2019Review
- Consequences of BMPR2 Deficiency in the Pulmonary Vasculature and Beyond: Contributions to Pulmonary Arterial Hypertension.International journal of molecular sciences · 2018Review
- The role of extracellular matrix stiffness in megakaryocyte and platelet development and function.American journal of hematology · 2018Review
- Megakaryocyte Contribution to Bone Marrow Fibrosis: many Arrows in the Quiver.Mediterranean journal of hematology and infectious diseases · 2018Review
- The role of the extracellular matrix in primary myelofibrosis.Blood cancer journal · 2017Review
- Bone marrow fibrosis in myelofibrosis: pathogenesis, prognosis and targeted strategies.Haematologica · 2016Review
- Myeloproliferative neoplasms and inflammation: whether to target the malignant clone or the inflammatory process or both.Leukemia · 2016Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary myelofibrosis (PMF) is a myeloproliferative neoplasia characterized by progressive deposition of extracellular matrix components in the bone marrow. The involvement of members of the bone morphogenetic protein (BMP) family in aberrant bone marrow matrix homeostasis in PMF has not yet been investigated. Therefore, we analyzed expression of BMP1, an activator of latent transforming growth factor beta-1 (TGFbeta-1) and processor of collagen precursors, and other BMPs in bone marrow from PMF patients and controls (n = 95). Expression of BMP1, BMP6, BMP7, and BMP-receptor 2 was significantly increased in advanced stages of myelofibrosis compared with controls (P < or = 0.01), and enhanced levels of BMP6 expression were already evident in prefibrotic stages of PMF. Immunohistochemistry showed that bone marrow stromal cells and megakaryocytes were the major cellular sources of BMP1 protein. Because TGFbeta-1 and basic fibroblast growth factor have been shown to be important in the development of myelofibrosis, we studied the induction of BMPs by these cytokines in cultured fibroblasts. Fibroblasts treated with TGFbeta-1 showed a pronounced up-regulation of BMP6, suggesting that stromal cells may be susceptible to BMP activation by cytokines with a proven role in the pathogenesis of PMF. We conclude that BMP family members may play an important role in the pathogenesis of myelofibrosis in PMF and are apparently induced by cytokines such as TGFbeta-1.
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