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Cited by 80Wound Healing and TreatmentsInflammation biomarkers and pathwaysLiver physiology and pathology

Cytokine gene expression in a murine wound healing model

Bryan, Donna, Walker, Kenneth B., Ferguson, Mark, Thorpe, Robin·2005·Cytokine
DOI 10.1016/j.cyto.2005.06.015
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Abstract

Inflammatory mediators have been shown to play a major role in the complex series of co-ordinated events that occur in wound healing responses following injury. However, to date most of the studies carried out have addressed the expression, interactions and role of only one or two cytokines that are thought to be involved in wound repair. This study has evaluated, in murine skin samples taken at 0, 3, 12, 18, 24, 48, 72, 120 and 168 h post-wounding, the expression of a wide range of cytokines with potential for a role in wound repair. Various techniques (reverse transcription polymerase chain reaction (RT-PCR), bioassays and ELISA) were used to evaluate cytokine expression in these samples at both the mRNA and protein expressions level. Semi-quantitative analysis using RT-PCR revealed that IL-1beta, IP10, bFGF, and TGFbeta3 up-regulated in wounded samples, compared to non-injured control samples. Expression of mRNA for other cytokines and inflammatory mediators, IL-1alpha, IL-6, TGFbeta1, TNFalpha, MIP-1alpha, MIP-2, JE, KC, PDGFalpha and PDGFbeta, were found to be down-regulated in injured adult murine samples compared to normal control samples. Interestingly we failed to find evidence of mRNA expression for the cytokines IL-2, IL-4, IL-12, GM-CSF, IFNgamma and RANTES, in both non-injured and injured samples. These observations were also generally supported by the results obtained using bioassays for IL-1 and IL-6 and ELISA for IL-1alpha, IL-1beta, IL-6, TNFalpha, and IFNgamma.

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Crossref · 10.1016/j.cyto.2005.06.015

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  • In mouse skin wounds, IL-4 mRNA and protein are not detectable at early or late time-points.

    “In mouse skin wounds, IL-4 mRNA and protein are not detectable at early or late time-points [60,71].”

    From Macrophage phenotypes during tissue repair (2013) · cites this paper as [71]

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Authors
Bryan, D., Walker, K. B., Ferguson, M., & Thorpe, R.
Affiliations
  • National Institute for Biological Standards and Control (GB)
  • University of Manchester (GB)
Corresponding author
Bryan, Donna
ORCID
Ferguson, Mark
Venue
Cytokine
Publisher
Elsevier BV
Published
2005-09
Volume
31
Issue
6
Pages
429-438
ISSN
1043-4666 (ISSN-L)
DOI
10.1016/j.cyto.2005.06.015
OpenAlex
W1999878829
Cited by
80
References
66
Citations by year
2024: 3 · 2023: 3 · 2022: 3 · 2021: 2 · 2020: 1 · 2019: 2 · 2018: 4 · 2017: 8 · 2016: 2 · 2015: 2 · 2014: 6 · 2013: 5 · 2012: 9
FWCI
3.89
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Cytokine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
  • Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords
wound healing, cytokine gene expression, skin damage, mouse model, IL-1β, interleukin-6, TNF-α, TGF-beta3, basic fibroblast growth factor, CXCL10, inflammatory mediators, cytokine mRNA expression
MeSH terms
Animals, Biological Assay, Cell Line, Enzyme-Linked Immunosorbent Assay, Male, Mice, Inbred Strains, RNA, Messenger, Wound Healing, Gene Expression, Cytokines, Reverse Transcriptase Polymerase Chain Reaction, Models, Animal, Mice

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