Evidence map›Paper›PMID 10951241›Full record

ArticleThe Journal of investigative dermatology2000

Delayed wound healing in CXCR2 knockout mice.

R M Devalaraja, L B Nanney, J Du, Q Qian, Y Yu, M N Devalaraja, A Richmond

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 188 papers.

0numbers the graph read from it
0cells of the map it votes in
188citing papers in PubMed
17.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

188 citing papers in PubMed, 425 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Apoptosis and Cell Clearance in Skin Wound Healing.Advances in experimental medicine and biology · 2025
    Review

128 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

7 authors at 1 institution in 2 countries.

R M DevalarajaDepartments of Cell Biology, Plastic Surgery, Medicine (Division of Dermatology), Vanderbilt University School of Medicine and Department of Veterans Affairs, Nashville, Tennessee 37232, USA.
L B Nanney
J Du
Q Qian
Y Yu
M N Devalaraja
A Richmond
Tennessee Department of Education · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
MELANOMA GROWTH STIMULATORY ACTIVITYR01CA034590 · NCI · VANDERBILT UNIVERSITY · PI RICHMOND, ANN · 1986 to 2017
$5.2M
BIOCHEMIISTRY OF A MELANOMA GROWTH STIMULATIONR23CA034590 · NCI · EMORY UNIVERSITY · PI RICHMOND, ANN · 1985 to 1985
–
BLRD VA IK6 BX005225NCI NIH HHS CA34590NCI NIH HHS CA68485NCI NIH HHS P30 CA068485NCI NIH HHS R01 CA034590NIAMS NIH HHS 5P30AR4194
6 · The paper itself

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.

Indexed as

AnimalsCell MovementCytokinesKeratinocytesMiceMice, Inbred BALB CMice, KnockoutMonocytesNeovascularization, PhysiologicNeutrophilsReceptors, ChemokineReceptors, InterleukinReceptors, Interleukin-8BSkinTime FactorsWound HealingCytokinesReceptors, ChemokineReceptors, InterleukinReceptors, Interleukin-8B

Identifiers

PMID10951241
PMCPMC2664868
OpenAlexW2001356286

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.