دورية أكاديمية
Aged marrow macrophages expand platelet-biased hematopoietic stem cells via Interleukin1B.
| العنوان: | Aged marrow macrophages expand platelet-biased hematopoietic stem cells via Interleukin1B. |
|---|---|
| المؤلفون: | Frisch BJ; Department of Medicine.; James P. Wilmot Cancer Institute, and., Hoffman CM; Department of Medicine.; James P. Wilmot Cancer Institute, and.; Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA., Latchney SE; Department of Medicine.; James P. Wilmot Cancer Institute, and., LaMere MW; Department of Medicine.; James P. Wilmot Cancer Institute, and., Myers J; James P. Wilmot Cancer Institute, and.; UR Genomics Research Center, Rochester, New York, USA., Ashton J; James P. Wilmot Cancer Institute, and.; UR Genomics Research Center, Rochester, New York, USA., Li AJ; Department of Medicine.; James P. Wilmot Cancer Institute, and., Saunders J 2nd; Center for Pediatric Biomedical Research and.; Department of Pathology and Laboratory Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA., Palis J; James P. Wilmot Cancer Institute, and.; Center for Pediatric Biomedical Research and., Perkins AS; James P. Wilmot Cancer Institute, and.; Department of Pathology and Laboratory Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA., McCabe A; Department of Immunology and Microbial Disease, Albany Medical College, Albany, New York, USA., Smith JN; Department of Immunology and Microbial Disease, Albany Medical College, Albany, New York, USA., McGrath KE; Center for Pediatric Biomedical Research and., Rivera-Escalera F; Department of Microbiology and Immunology., McDavid A; Department of Biostatistics and Computational Biology, and., Liesveld JL; Department of Medicine.; James P. Wilmot Cancer Institute, and., Korshunov VA; Department of Medicine.; Aab Cardiovascular Research Institute, University of Rochester Medical Center, Rochester, New York, USA., Elliott MR; Department of Microbiology and Immunology., MacNamara KC; Department of Immunology and Microbial Disease, Albany Medical College, Albany, New York, USA., Becker MW; Department of Medicine.; James P. Wilmot Cancer Institute, and., Calvi LM; Department of Medicine.; James P. Wilmot Cancer Institute, and. |
| المصدر: | JCI insight [JCI Insight] 2019 Apr 18; Vol. 5. Date of Electronic Publication: 2019 Apr 18. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. |
| اللغة: | English |
| بيانات الدورية: | Publisher: American Society for Clinical Investigation Country of Publication: United States NLM ID: 101676073 Publication Model: Electronic Cited Medium: Internet ISSN: 2379-3708 (Electronic) Linking ISSN: 23793708 NLM ISO Abbreviation: JCI Insight Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Ann Arbor, Michigan : American Society for Clinical Investigation, [2016]- |
| مواضيع طبية MeSH: | Aging/*physiology , Blood Platelets/*metabolism , Bone Marrow/*metabolism , Hematopoietic Stem Cells/*metabolism , Interleukin-1beta/*metabolism , Macrophages/*metabolism, Animals ; Bone Marrow/pathology ; Caspase 1/metabolism ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neutrophils ; Phagocytosis ; Phenotype ; Proto-Oncogene Proteins ; Receptor Protein-Tyrosine Kinases ; Axl Receptor Tyrosine Kinase |
| مستخلص: | The bone marrow microenvironment (BMME) contributes to the regulation of hematopoietic stem cell (HSC) function, though its role in age-associated lineage skewing is poorly understood. Here we show that dysfunction of aged marrow macrophages (Mφs) directs HSC platelet-bias. Mφs from the marrow of aged mice and humans exhibited an activated phenotype, with increased expression of inflammatory signals. Aged marrow Mφs also displayed decreased phagocytic function. Senescent neutrophils, typically cleared by marrow Mφs, were markedly increased in aged mice, consistent with functional defects in Mφ phagocytosis and efferocytosis. In aged mice, Interleukin 1B (IL1B) was elevated in the bone marrow and caspase 1 activity, which can process pro-IL1B, was increased in marrow Mφs and neutrophils. Mechanistically, IL1B signaling was necessary and sufficient to induce a platelet bias in HSCs. In young mice, depletion of phagocytic cell populations or loss of the efferocytic receptor Axl expanded platelet-biased HSCs. Our data support a model wherein increased inflammatory signals and decreased phagocytic function of aged marrow Mφs induce the acquisition of platelet bias in aged HSCs. This work highlights the instructive role of Mφs and IL1B in the age-associated lineage-skewing of HSCs, and reveals the therapeutic potential of their manipulation as antigeronic targets. |
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| معلومات مُعتمدة: | R01 DK098251 United States DK NIDDK NIH HHS; P30 AR069655 United States AR NIAMS NIH HHS; F32 CA180615 United States CA NCI NIH HHS; U01 AI107276 United States AI NIAID NIH HHS; R01 AI114554 United States AI NIAID NIH HHS; K12 GM106997 United States GM NIGMS NIH HHS; F31 HL131184 United States HL NHLBI NIH HHS; R01 AG046293 United States AG NIA NIH HHS; R01 GM105949 United States GM NIGMS NIH HHS; R01 CA166280 United States CA NCI NIH HHS; F30 DK113727 United States DK NIDDK NIH HHS |
| فهرسة مساهمة: | Keywords: Aging; Bone marrow; Hematology; Hematopoietic stem cells |
| المشرفين على المادة: | 0 (IL1B protein, human) 0 (IL1B protein, mouse) 0 (Interleukin-1beta) 0 (Proto-Oncogene Proteins) EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases) EC 3.4.22.36 (Caspase 1) 0 (Axl Receptor Tyrosine Kinase) |
| تواريخ الأحداث: | Date Created: 20190419 Date Completed: 20200914 Latest Revision: 20221207 |
| رمز التحديث: | 20240628 |
| مُعرف محوري في PubMed: | PMC6542605 |
| DOI: | 10.1172/jci.insight.124213 |
| PMID: | 30998506 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 2379-3708 |
|---|---|
| DOI: | 10.1172/jci.insight.124213 |