ArticleEMBO molecular medicine2023
Disease modification and symptom relief in osteoarthritis using a mutated GCP-2/CXCL6 chemokine.
Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Mastication-Induced Electrical Stimulation Activates Prg4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Machine Learning-Based Identification of Molecular Signatures in PTOA Cell Subtypes via Single-Cell Transcriptomics in a Mouse Model.Stem cell reviews and reports · 2026Article
- Integrated machine learning and single-cell RNA sequencing reveal COL4A2 and CXCL6 as oxidative stress-associated biomarkers in periodontitis.Frontiers in immunology · 2025Article
- CXCR2 chemokine receptor - a master regulator in cancer and physiology.Trends in molecular medicine · 2024Review
- Chemokines in Cartilage Regeneration and Degradation: New Insights.International journal of molecular sciences · 2023Review
- The role of CXCL family members in different diseases.Cell death discovery · 2023Review
- Disease modification and symptom relief in osteoarthritis using a mutated GCP-2/CXCL6 chemokine.EMBO molecular medicine · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
24 authors at 5 institutions in 4 countries.
Funding
Abstract
We showed that the chemokine receptor C-X-C Motif Chemokine Receptor 2 (CXCR2) is essential for cartilage homeostasis. Here, we reveal that the CXCR2 ligand granulocyte chemotactic protein 2 (GCP-2) was expressed, during embryonic development, within the prospective permanent articular cartilage, but not in the epiphyseal cartilage destined to be replaced by bone. GCP-2 expression was retained in adult articular cartilage. GCP-2 loss-of-function inhibited extracellular matrix production. GCP-2 treatment promoted chondrogenesis in vitro and in human cartilage organoids implanted in nude mice in vivo. To exploit the chondrogenic activity of GCP-2, we disrupted its chemotactic activity, by mutagenizing a glycosaminoglycan binding sequence, which we hypothesized to be required for the formation of a GCP-2 haptotactic gradient on endothelia. This mutated version (GCP-2-T) had reduced capacity to induce transendothelial migration in vitro and in vivo, without affecting downstream receptor signaling through AKT, and chondrogenic activity. Intra-articular adenoviral overexpression of GCP-2-T, but not wild-type GCP-2, reduced pain and cartilage loss in instability-induced osteoarthritis in mice. We suggest that GCP-2-T may be used for disease modification in osteoarthritis.
Indexed as
Identifiers
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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.