Cited by 429Wound Healing and TreatmentsChemokine receptors and signalingInflammation biomarkers and pathways

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Delayed Wound Healing in CXCR2 Knockout Mice

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Devalaraja, Radhika M., Nanney, Lillian B., Qian, Qinghua, Du, Jianguo, Yu, Yingchun, Devalaraja, Madhav N., Richmond, Ann·2000·Journal of Investigative Dermatology

DOI 10.1046/j.1523-1747.2000.00034.xPMC PMC2664868

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Abstract

Previous studies demonstrated that the CXC chemokine, MGSA/GRO-alpha and its receptor, CXCR2, are expressed during wound healing by keratinocytes and endothelial cells at areas where epithelialization and neovascularization occur. The process of wound healing is dependent on leukocyte recruitment, keratinocyte proliferation and migration, and angiogenesis. These processes may be mediated in part by CXC chemokines, such as interleukin-8 and MGSA/GRO-alpha. To examine further the significance of CXC chemokines in wound healing, full excisional wounds were created on CXCR2 wild-type (+/+), heterozygous (+/-), or knockout (-/-) mice. Wounds were histologically analyzed for neutrophil and monocyte infiltration, neovascularization and epithelialization at days 3, 5, 7, and 10 postwounding. The CXCR2 -/- mice exhibited defective neutrophil recruitment, an altered temporal pattern of monocyte recruitment, and altered secretion of interleukin-1beta. Significant delays in wound healing parameters, including epithelialization and decreased neovascularization, were also observed in CXCR2 -/- mice. In vitro wounding experiments with cultures of keratinocytes established from -/- and +/+ mice revealed a retardation in wound closure in CXCR2 -/- keratinocytes, suggesting a role for this receptor on keratinocytes in epithelial resurfacing that is independent of neutrophil recruitment. These in vitro and in vivo studies further establish a pathophysiologic role for CXCR2 during cutaneous wound repair.

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Authors: Devalaraja, R. M., Nanney, L. B., Qian, Q., Du, J., Yu, Y., Devalaraja, M. N., & Richmond, A.
Affiliations: Vanderbilt University (US)
United States Department of Veterans Affairs (US)
Corresponding author: Richmond, Ann
ORCID: Yu, Yingchun
Richmond, Ann
Venue: Journal of Investigative Dermatology
Publisher: Elsevier BV
Published: 2000-08
Volume: 115
Issue: 2
Pages: 234-244
ISSN: 0022-202X (ISSN-L)
DOI: 10.1046/j.1523-1747.2000.00034.x
PMC: PMC2664868
OpenAlex: W2001356286
Cited by: 429
References: 50
Citations by year: 2026: 7 · 2025: 13 · 2024: 17 · 2023: 15 · 2022: 17 · 2021: 23 · 2020: 21 · 2019: 17 · 2018: 12 · 2017: 27 · 2016: 10 · 2015: 23 · 2014: 15 · 2013: 19 · 2012: 12
FWCI: 15.79
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 5601 d)
Locations: Journal of Investigative Dermatology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: U.S. Department of Veterans Affairs (IK6 BX005225)
National Cancer Institute (CA 34590, CA68485, R01CA034590, P30CA068485)
National Institute of Arthritis and Musculoskeletal and Skin Diseases (5P30 AR4194)
Topics: Health Sciences › Medicine › Surgery › Wound Healing and Treatments
Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Keywords: CXCR2, delayed wound healing, CXC chemokines, CXCL1, interleukin-8, keratinocytes, neutrophil recruitment, monocyte recruitment, neovascularization, re-epithelialization, IL-1β, excision wound, skin wound healing, knockout mice
MeSH terms: Animals, Cell Movement, Mice, Inbred BALB C, Monocytes, Neutrophils, Skin, Time Factors, Wound Healing, Wounds and Injuries, Keratinocytes, Cytokines, Receptors, Interleukin, Mice, Knockout, Neovascularization, Physiologic, Receptors, Chemokine, Receptors, Interleukin-8B, Mice

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Delayed Wound Healing in CXCR2 Knockout Mice

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