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

The DOI matches its Crossref record; 48 of the 50 references it cites were found in a registry or an index.

Delayed Wound Healing in CXCR2 Knockout Mice

Open access
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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Crossref · 10.1046/j.1523-1747.2000.00034.x

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Research works printed but not linked: 2

  1. Leibovitch, 1975, The role of macrophage in wound repair, Am J Pathol, 78, 71
  2. Riches, 1996, Differential regulation of pro-inflammatory cytokines during wound healing in normal and glucocorticoid-treated mice, Cytokine, 8, 548, 10.1006/cyto.1996.0074 · DOI

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Metadata

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
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
Licence
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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