ArticleThe Journal of clinical investigation2017
Endothelial jagged-2 sustains hematopoietic stem and progenitor reconstitution after myelosuppression.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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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.
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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
58 citing papers in PubMed, 80 citations in OpenAlex.
- Spatially resolved multiomics of human meningeal development reveal lineage and disease dynamics.Nature cell biology · 2026Article
- Bone Lymphatic Endothelial Cells Form a Distinct Skeletal Population and Drive Skeletal Repair.bioRxiv : the preprint server for biology · 2026Article
- Identifying NOTCH signaling-specialized hematopoietic supportive subpopulation from mesenchymal stem cells.Stem cell research & therapy · 2026Article
- The bone marrow niche and hematopoietic system are distinctly remodeled by CD45-targeted astatine-211 radioimmunotherapy.Blood advances · 2026Article
- Jagged-mediated lateral induction patterns Notch3 signaling within adult neural stem cell populations.Nature communications · 2026Article
- Specialized Pulmonary Vascular Cells in Development and Disease.Annual review of physiology · 2025Review
- Bone marrow adipocytes: key players in vascular niches, aging, and disease.Frontiers in cell and developmental biology · 2025Review
- Bone marrow niches for hematopoietic stem cells.HemaSphere · 2024Review
- Systemic and local regulation of hematopoietic homeostasis in health and disease.Nature cardiovascular research · 2024Review
- 2Molecular imaging and biology · 2024Article
- The evolving hematopoietic niche during development.Frontiers in molecular biosciences · 2024Review
- Article
- Pathological angiogenesis: mechanisms and therapeutic strategies.Angiogenesis · 2023Review
- Further Characterization of Multi-Organ DEARE and Protection by 16,16 Dimethyl Prostaglandin E2 in a Mouse Model of the Hematopoietic Acute Radiation Syndrome.Radiation research · 2023Article
- Notch Signaling in the Vasculature: Angiogenesis and Angiocrine Functions.Cold Spring Harbor perspectives in medicine · 2023Review
- Article
- Mesenchymal stromal cells, metabolism, and mitochondrial transfer in bone marrow normal and malignant hematopoiesis.Frontiers in cell and developmental biology · 2023Review
- Aging, Causes, and Rejuvenation of Hematopoietic Stem Cells.Advances in experimental medicine and biology · 2023Article
- Systems Biology Analysis of Temporal Dynamics That Govern Endothelial Response to Cyclic Stretch.Biomolecules · 2022Review
- The cellular composition and function of the bone marrow niche after allogeneic hematopoietic cell transplantation.Bone marrow transplantation · 2022Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Angiocrine factors, such as Notch ligands, supplied by the specialized endothelial cells (ECs) within the bone marrow and splenic vascular niche play an essential role in modulating the physiology of adult hematopoietic stem and progenitor cells (HSPCs). However, the relative contribution of various Notch ligands, specifically jagged-2, to the homeostasis of HSPCs is unknown. Here, we show that under steady state, jagged-2 is differentially expressed in tissue-specific vascular beds, but its expression is induced in hematopoietic vascular niches after myelosuppressive injury. We used mice with EC-specific deletion of the gene encoding jagged-2 (Jag2) to demonstrate that while EC-derived jagged-2 was dispensable for maintaining the capacity of HSPCs to repopulate under steady-state conditions, by activating Notch2 it did contribute to the recovery of HSPCs in response to myelosuppressive conditions. Engraftment and/or expansion of HSPCs was dependent on the expression of endothelial-derived jagged-2 following myeloablation. Additionally, jagged-2 expressed in bone marrow ECs regulated HSPC cell cycle and quiescence during regeneration. Endothelial-deployed jagged-2 triggered Notch2/Hey1, while tempering Notch2/Hes1 signaling in HSPCs. Collectively, these data demonstrate that EC-derived jagged-2 activates Notch2 signaling in HSPCs to promote hematopoietic recovery and has potential as a therapeutic target to accelerate balanced hematopoietic reconstitution after myelosuppression.
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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.