ArticlePhysiological reports2021
Active hematopoiesis triggers exosomal release of PRDX2 that promotes osteoclast formation.
Article in Physiological reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Advances in understanding exosome-mediated regulation of macrophage function.Frontiers in immunology · 2026Review
- Effects of exosomes from different origins on osteoclasts.Journal of orthopaedic surgery and research · 2025Review
- Targeting lipid raft-related stomatin to ameliorate osteoporosis in preclinical models.Nature communications · 2025Article
- Transforming the Niche: The Emerging Role of Extracellular Vesicles in Acute Myeloid Leukaemia Progression.International journal of molecular sciences · 2024Review
- Cellular and Molecular Connections Between Bone Fracture Healing and Exosomes.Physiological research · 2023Review
- Peroxiredoxin 2: An Important Element of the Antioxidant Defense of the Erythrocyte.Antioxidants (Basel, Switzerland) · 2023Review
- Coordinated reprogramming of renal cancer transcriptome, metabolome and secretome associates with immune tumor infiltration.Cancer cell international · 2023Article
- Erythropoietin Receptor (EPOR) Signaling in the Osteoclast Lineage Contributes to EPO-Induced Bone Loss in Mice.International journal of molecular sciences · 2022Article
- Mechanical force-promoted osteoclastic differentiation via periodontal ligament stem cell exosomal protein ANXA3.Stem cell reports · 2022Article
- The Non-Erythropoietic EPO Analogue Cibinetide Inhibits Osteoclastogenesis In Vitro and Increases Bone Mineral Density in Mice.International journal of molecular sciences · 2021Article
- Effect of Erythropoietin on the Expression of Murine Transferrin Receptor 2.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Hematopoietic disorders, particularly hemolytic anemias, commonly lead to bone loss. We have previously reported that actively proliferating cancer cells stimulate osteoclastogenesis from late precursors in a RANKL-independent manner. We theorized that cancer cells exploit the physiological role of bone resorption to support expanding hematopoietic bone marrow and examined if hematopoietic cells can trigger osteoclastogenesis. Using phlebotomy-induced acute anemia in mice, we found strong correlation between augmented erythropoiesis and increased osteoclastogenesis. Conditioned medium (CM) from K562 erythroleukemia cells and primary mouse erythroblasts stimulated osteoclastogenesis when added to RANKL-primed precursors from mouse bone marrow or RAW264.7 cells. Using immunoblotting and mass spectrometry, PRDX2 was identified as a factor produced by erythroid cells in vitro and in vivo. PRDX2 was detected in K562-derived exosomes, and inhibiting exosomal release significantly decreased the osteoclastogenic capacity of K562 CM. Recombinant PRDX2 induced osteoclast formation from RANKL-primed primary or RAW 264.7 precursors to levels comparable to achieved with continuous RANKL treatment. Thus, increased bone marrow erythropoiesis secondary to anemia leads to upregulation of PRDX2, which is released in the exosomes and acts to induce osteoclast formation. Increased bone resorption by the osteoclasts expands bone marrow cavity, which likely plays a supporting role to increase blood cell production.
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Registered trials
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