ArticleJournal of cell science2009
IP-10 induces dissociation of newly formed blood vessels.
Article in Journal of cell science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 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
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Who cites it
79 citing papers in PubMed, 140 citations in OpenAlex.
- Modulation of Chemokine Activity for Enhanced Angiogenesis and Tissue Regeneration in Chronic Wounds.International journal of molecular sciences · 2026Review
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- Homeostatic Regulation of Pro-Angiogenic and Anti-Angiogenic Proteins via Hedgehog, Notch Grid, and Ephrin Signaling in Tibial Dyschondroplasia.Animals : an open access journal from MDPI · 2023Review
- IDO1 and inflammatory neovascularization: bringing new blood to tumor-promoting inflammation.Frontiers in oncology · 2023Review
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- CXCR3 deletion aggravates corneal neovascularization in a corneal alkali-burn model.Experimental eye research · 2022Article
- Physiological and Pathological Remodeling of Cerebral Microvessels.International journal of molecular sciences · 2022Review
- Angiogenesis in Wound Repair: Too Much of a Good Thing?Cold Spring Harbor perspectives in biology · 2022Review
- T cell apoptosis characterizes severe Covid-19 disease.Cell death and differentiation · 2022Article
- Role of CXCL10 in Spinal Cord Injury.International journal of medical sciences · 2022Review
- Lymphatic Vessel Regression and Its Therapeutic Applications: Learning From Principles of Blood Vessel Regression.Frontiers in physiology · 2022Review
- Oxidized carbon black nanoparticles induce endothelial damage through C-X-C chemokine receptor 3-mediated pathway.Redox biology · 2021Article
- Review
- Pro- and Antiangiogenic Factors in Gliomas: Implications for Novel Therapeutic Possibilities.International journal of molecular sciences · 2021Review
- The cytokine storm in COVID-19: Further advances in our understanding the role of specific chemokines involved.Cytokine & growth factor reviews · 2021Review
- Dephosphorylation of Caveolin-1 Controls C-X-C Motif Chemokine Ligand 10 Secretion in Mesenchymal Stem Cells to Regulate the Process of Wound Healing.Frontiers in cell and developmental biology · 2021Article
- Umbilical cord-derived mesenchymal stem cells preconditioned with isorhamnetin: potential therapy for burn wounds.World journal of stem cells · 2020Article
- Two distinct immunopathological profiles in autopsy lungs of COVID-19.Nature communications · 2020Article
- Tumor-on-a-chip platform to interrogate the role of macrophages in tumor progression.Integrative biology : quantitative biosciences from nano to macro · 2020Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The signals that prune the exuberant vascular growth of tissue repair are still ill defined. We demonstrate that activation of CXC chemokine receptor 3 (CXCR3) mediates the regression of newly formed blood vessels. We present evidence that CXCR3 is expressed on newly formed vessels in vivo and in vitro. CXCR3 is expressed on vessels at days 7-21 post-wounding, and is undetectable in unwounded or healed skin. Treatment of endothelial cords with CXCL10 (IP-10), a CXCR3 ligand present during the resolving phase of wounds, either in vitro or in vivo caused dissociation even in the presence of angiogenic factors. Consistent with this, mice lacking CXCR3 express a greater number of vessels in wound tissue compared to wild-type mice. We then hypothesized that signaling from CXCR3 not only limits angiogenesis, but also compromises vessel integrity to induce regression. We found that activation of CXCR3 triggers micro-calpain activity, causing cleavage of the cytoplasmic tail of beta3 integrins at the calpain cleavage sites c'754 and c'747. IP-10 stimulation also activated caspase 3, blockage of which prevented cell death but not cord dissociation. This is the first direct evidence for an extracellular signaling mechanism through CXCR3 that causes the dissociation of newly formed blood vessels followed by cell death.
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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.