ArticleThe Journal of biological chemistry2015
The Positively Charged COOH-terminal Glycosaminoglycan-binding CXCL9(74-103) Peptide Inhibits CXCL8-induced Neutrophil Extravasation and Monosodium Urate Crystal-induced Gout in Mice.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 62 citations in OpenAlex.
- Dynamic regulation and targeted intervention of neutrophils in hepatic ischemia‑reperfusion injury (Review).International journal of molecular medicine · 2026Review
- Molecular basis of CXC chemokine receptor 3 ligand multispecificity.Science advances · 2026Article
- Chemokines CXCL9 and CCL2 in Relation to Cerebral White Matter Disease, Cognitive Decline, and Dementia: The Northern Manhattan Study.Neurology open access · 2026Article
- Monitoring T-Cell Activation in the Tumor Microenvironment by PET Imaging of the Chemokine CXCL9.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025Article
- Migration arrest and transendothelial trafficking of human pathogenic-like Th17 cells are mediated by differentially positioned chemokines.Nature communications · 2025Article
- The glycosaminoglycan-binding chemokine fragment CXCL9(74-103) reduces inflammation and tissue damage in mouse models of coronavirus infection.Frontiers in immunology · 2024Article
- Chemokines form complex signals during inflammation and disease that can be decoded by extracellular matrix proteoglycans.Science signaling · 2023Article
- Chemokine positioning determines mutually exclusive roles for their receptors in extravasation of pathogenic human T cells.bioRxiv : the preprint server for biology · 2023Article
- Mechanism of ShuiJingDan in Treating Acute Gouty Arthritis Flares Based on Network Pharmacology and Molecular Docking.Drug design, development and therapy · 2023Article
- CXCL17 binds efficaciously to glycosaminoglycans with the potential to modulate chemokine signaling.Frontiers in immunology · 2023Article
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- The GAG-Binding Peptide MIG30 Protects against Liver Ischemia-Reperfusion in Mice.International journal of molecular sciences · 2022Article
- The Therapeutic Treatment with the GAG-Binding Chemokine Fragment CXCL9(74-103) Attenuates Neutrophilic Inflammation and Lung Dysfunction duringInternational journal of molecular sciences · 2022Article
- CXCL8, CXCL9, CXCL10, and CXCL11 as biomarkers of liver injury caused by chronic hepatitis B.Frontiers in microbiology · 2022Article
- Inhibition of renal fibrosis with a human CXCL9-derived glycosaminoglycan-binding peptide.Clinical & translational immunology · 2022Article
- Affinity and Specificity for Binding to Glycosaminoglycans Can Be Tuned by Adapting Peptide Length and Sequence.International journal of molecular sciences · 2021Article
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- S. mansoni SmKI-1 Kunitz-domain: Leucine point mutation at P1 site generates enhanced neutrophil elastase inhibitory activity.PLoS neglected tropical diseases · 2021Article
- Understanding the mechanisms that facilitate specificity, not redundancy, of chemokine-mediated leukocyte recruitment.Immunology · 2020Review
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ELR(-)CXC chemokine CXCL9 is characterized by a long, highly positively charged COOH-terminal region, absent in most other chemokines. Several natural leukocyte- and fibroblast-derived COOH-terminally truncated CXCL9 forms missing up to 30 amino acids were identified. To investigate the role of the COOH-terminal region of CXCL9, several COOH-terminal peptides were chemically synthesized. These peptides display high affinity for glycosaminoglycans (GAGs) and compete with functional intact chemokines for GAG binding, the longest peptide (CXCL9(74-103)) being the most potent. The COOH-terminal peptide CXCL9(74-103) does not signal through or act as an antagonist for CXCR3, the G protein-coupled CXCL9 receptor, and does not influence neutrophil chemotactic activity of CXCL8 in vitro. Based on the GAG binding data, an anti-inflammatory role for CXCL9(74-103) was further evidenced in vivo. Simultaneous intravenous injection of CXCL9(74-103) with CXCL8 injection in the joint diminished CXCL8-induced neutrophil extravasation. Analogously, monosodium urate crystal-induced neutrophil migration to the tibiofemural articulation, a murine model of gout, is highly reduced by intravenous injection of CXCL9(74-103). These data show that chemokine-derived peptides with high affinity for GAGs may be used as anti-inflammatory peptides; by competing with active chemokines for binding and immobilization on GAGs, these peptides may lower chemokine presentation on the endothelium and disrupt the generation of a chemokine gradient, thereby preventing a chemokine from properly performing its chemotactic function. The CXCL9 peptide may serve as a lead molecule for further development of inhibitors of inflammation based on interference with chemokine-GAG interactions.
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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.