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• W2912561801 abstract "The fibronectin EDA isoform (EDA FN) is instrumental in fibrogenesis but, to date, its expression and function in bone marrow (BM) fibrosis have not been explored. We found that mice constitutively expressing the EDA domain (EIIIA+/+), but not EDA knockout mice, are more prone to develop BM fibrosis upon treatment with the thrombopoietin (TPO) mimetic romiplostim (TPOhigh). Mechanistically, EDA FN binds to TLR4 and sustains progenitor cell proliferation and megakaryopoiesis in a TPO-independent fashion, inducing LPS-like responses, such as NF-κB activation and release of profibrotic IL-6. Pharmacological inhibition of TLR4 or TLR4 deletion in TPOhigh mice abrogated Mk hyperplasia, BM fibrosis, IL-6 release, extramedullary hematopoiesis, and splenomegaly. Finally, developing a novel ELISA assay, we analyzed samples from patients affected by primary myelofibrosis (PMF), a well-known pathological situation caused by altered TPO signaling, and found that the EDA FN is increased in plasma and BM biopsies of PMF patients as compared with healthy controls, correlating with fibrotic phase." @default.
• W2912561801 created "2019-02-21" @default.
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• W2912561801 date "2019-02-07" @default.
• W2912561801 modified "2023-10-17" @default.
• W2912561801 title "EDA fibronectin–TLR4 axis sustains megakaryocyte expansion and inflammation in bone marrow fibrosis" @default.
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• W2912561801 doi "https://doi.org/10.1084/jem.20181074" @default.
• W2912561801 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6400533" @default.
• W2912561801 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30733282" @default.
• W2912561801 hasPublicationYear "2019" @default.
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