ArticleThe American journal of pathology2008
ELR-negative CXC chemokine CXCL11 (IP-9/I-TAC) facilitates dermal and epidermal maturation during wound repair.
Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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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Who cites it
37 citing papers in PubMed, 52 citations in OpenAlex.
- Development of a High-throughput Morphological Assay for Evaluating Mesenchymal Stromal Cell-derived Extracellular Vesicle Modulation of Brain Pericyte Secretory Phenotype.Stem cell reviews and reports · 2025Article
- Network analyses reveal new insights into the effect of multicomponent Tr14 compared to single-component diclofenac in an acute inflammation model.Journal of inflammation (London, England) · 2023Article
- Growth Factor and Cytokine Delivery Systems for Wound Healing.Cold Spring Harbor perspectives in biology · 2022Review
- Injected Versus Sponge-Applied Mitomycin C (MMC) During Modified Trabeculectomy in New Zealand White Rabbit Model.Translational vision science & technology · 2020Article
- The Synthetic Dipeptide Pidotimod Shows a Chemokine-Like Activity through CXC Chemokine Receptor 3 (CXCR3).International journal of molecular sciences · 2019Article
- The Role of CXCR3 and Its Chemokine Ligands in Skin Disease and Cancer.Frontiers in medicine · 2018Review
- Multipotent stromal cells/mesenchymal stem cells and fibroblasts combine to minimize skin hypertrophic scarring.Stem cell research & therapy · 2017Article
- Chemokine Signaling during Midline Epithelial Seam Disintegration Facilitates Palatal Fusion.Frontiers in cell and developmental biology · 2017Article
- CXCL11 Expression by Keratinocytes Occurs Transiently Between Reaching Confluence and Cellular Compaction.Advances in wound care · 2016Article
- Chemokines in Wound Healing and as Potential Therapeutic Targets for Reducing Cutaneous Scarring.Advances in wound care · 2015Review
- The Role of Chemokines in Fibrotic Wound Healing.Advances in wound care · 2015Review
- CXCR3 in carcinoma progression.Histology and histopathology · 2015Review
- CXCR3 chemokine receptor enables local CD8(+) T cell migration for the destruction of virus-infected cells.Immunity · 2015Article
- Delayed cutaneous wound closure in HO-2 deficient mice despite normal HO-1 expression.Journal of cellular and molecular medicine · 2014Article
- CXCR3-independent actions of the CXC chemokine CXCL10 in the infarcted myocardium and in isolated cardiac fibroblasts are mediated through proteoglycans.Cardiovascular research · 2014Article
- Pericyte regulation of vascular remodeling through the CXC receptor 3.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- Chemokines and Their Receptors Are Key Players in the Orchestra That Regulates Wound Healing.Advances in wound care · 2013Review
- Targeting tumor cell motility as a strategy against invasion and metastasis.Trends in pharmacological sciences · 2013Review
- Article
- The Beginning of the End: CXCR3 Signaling in Late-Stage Wound Healing.Advances in wound care · 2012Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
In skin wounds, the chemokine CXCR3 receptor appears to play a key role in coordinating the switch from regeneration of the ontogenically distinct mesenchymal and epithelial compartments toward maturation. However, because CXCR3 equivalently binds four different ELR-devoid CXC chemokines (ie, PF4/CXCL4, IP-10/CXCL10, MIG/CXCL9, and IP-9/CXCL11), we sought to identify the ligand that coordinates epidermal coverage with the maturation of the underlying superficial dermis. Because CXCL11 (IP-9 or I-TAC) is produced by redifferentiating keratinocytes late in the regenerative phase when re-epithelialization is completed and matrix maturation ensues, we generated mice in which an antisense construct (IP-9AS) eliminated IP-9 expression during the wound-healing process. Both full and partial thickness excisional wounds were created and analyzed histologically throughout a 2-month period. Wound healing was impaired in the IP-9AS mice, with a hypercellular and immature dermis noted even after 60 days. Re-epithelialization was delayed with a deficient delineating basement membrane persisting in mice expressing the IP-9AS construct. Provisional matrix components persisted in the dermis, and the mature basement membrane components laminin V and collagen IV were severely diminished. Interestingly, the inflammatory response was not diminished despite IP-9/I-TAC being chemotactic for such cells. We conclude that IP-9 is a key ligand in the CXCR3 signaling system for wound repair, promoting re-epithelialization and modulating the maturation of the superficial dermis.
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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.