ArticleThe Journal of clinical investigation2021
ANGPTL2-containing small extracellular vesicles from vascular endothelial cells accelerate leukemia progression.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
- EGR1-associated inflammatory and neurovascular signatures suggest a potential link between migraine and ischemic stroke.The journal of headache and pain · 2026Article
- Exosomal ANGPTL2 in cerebrospinal fluid as a novel prognostic biomarker for primary central nervous system lymphoma.Frontiers in immunology · 2026Article
- Function of hematopoiesis and bone marrow niche in inflammation and non-hematopoietic diseases.Life medicine · 2025Review
- Small extracellular vesicles: crucial mediators for prostate cancer.Journal of nanobiotechnology · 2025Review
- Endocytic recycling is central to circadian collagen fibrillogenesis and disrupted in fibrosis.eLife · 2025Article
- Article
- Endothelial Cell Derived Extracellular Vesicles and Hematopoiesis.Radiation research · 2024Review
- Proteinase 3 depletion attenuates leukemia by promoting myeloid differentiation.Cell death and differentiation · 2024Article
- Transforming the Niche: The Emerging Role of Extracellular Vesicles in Acute Myeloid Leukaemia Progression.International journal of molecular sciences · 2024Review
- Cysteine- and glycine-rich protein 1 predicts prognosis and therapy response in patients with acute myeloid leukemia.Clinical and experimental medicine · 2024Article
- Endothelial-derived small extracellular vesicles support B-cell acute lymphoblastic leukemia development.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Review
- Leukocyte immunoglobulin-like receptor B2 overexpression as a promising therapeutic target and noninvasive screening biomarker for colorectal cancer.World journal of gastroenterology · 2023Article
- Interlukin-4 weakens resistance to stress injury and megakaryocytic differentiation of hematopoietic stem cells by inhibiting Psmd13 expression.Scientific reports · 2023Article
- The E3 ligase TRIM31 regulates hematopoietic stem cell homeostasis and MLL-AF9 leukemia.Haematologica · 2023Article
- Glucose partitioning in the bone marrow micro-environment in acute myeloid leukaemia.Leukemia · 2023Article
- KIM-1 augments hypoxia-induced tubulointerstitial inflammation through uptake of small extracellular vesicles by tubular epithelial cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- SIRT2 regulates extracellular vesicle-mediated liver-bone communication.Nature metabolism · 2023Article
- Role of the bone marrow vascular niche in chemotherapy for MLL-AF9-induced acute myeloid leukemia.Blood science (Baltimore, Md.) · 2023Article
- Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Small extracellular vesicles (SEVs) are functional messengers of certain cellular niches that permit noncontact cell communications. Whether niche-specific SEVs fulfill this role in cancer is unclear. Here, we used 7 cell type-specific mouse Cre lines to conditionally knock out Vps33b in Cdh5+ or Tie2+ endothelial cells (ECs), Lepr+ BM perivascular cells, Osx+ osteoprogenitor cells, Pf4+ megakaryocytes, and Tcf21+ spleen stromal cells. We then examined the effects of reduced SEV secretion on progression of MLL-AF9-induced acute myeloid leukemia (AML), as well as normal hematopoiesis. Blocking SEV secretion from ECs, but not perivascular cells, megakaryocytes, or spleen stromal cells, markedly delayed the leukemia progression. Notably, reducing SEV production from ECs had no effect on normal hematopoiesis. Protein analysis showed that EC-derived SEVs contained a high level of ANGPTL2, which accelerated leukemia progression via binding to the LILRB2 receptor. Moreover, ANGPTL2-SEVs released from ECs were governed by VPS33B. Importantly, ANGPTL2-SEVs were also required for primary human AML cell maintenance. These findings demonstrate a role of niche-specific SEVs in cancer development and suggest targeting of ANGPTL2-SEVs from ECs as a potential strategy to interfere with certain types of AML.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.