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TFPI from Erythroblasts Drives Heme Production in Central Macrophages Promoting Erythropoiesis in Polycythemia Vera

GSE224994 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2024/03/01 Platform GPL24247
Summary
Erythropoietic homeostasis is coordinated by erythroblast development and challenged by a number of genetic diseases including polycythemia vera. Erythroblasts and central macrophages form erythroblastic islands to provide a specific environment for erythropoiesis. However, how central macrophages interplay with erythroblasts during erythropoiesis remains to be further clarified. In this study, we found that erythroid-specific TFPI knockout decreased the number of erythroblasts under both steady-state and stress conditions, and the function of TFPI in erythropoiesis was mediated by macrophages. TFPI affects the downstream heme synthesis pathway of central macrophages, as shown by RNA sequencing analysis, and the deletion of TFPI reduced the heme content of macrophages by inhibiting ferrochelatase (Fech) expression. Our results show that TFPI plays an important role in the regulation of erythropoiesis and reveal a new mechanism of interplay between erythroblasts and macrophages. TFPI will also provide a new potential treatment strategy for polycythemia vera.
Published in
TFPI from erythroblasts drives heme production in central macrophages promoting erythropoiesis in polycythemia
Ma JK, Su LD, Feng LL et al. · Nature communications 2024 · PMID 38729948 · doi:10.1038/s41467-024-48328-8
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Also filed as BioProject PRJNA933340 and SRA study SRP421765. Searching any of these in the dataset finder brings you back here.

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