Role of P38 MAPK in UVB-Induced Inflammatory Responses in the Skin of SKH-1 Hairless Mice

Kim, Arianna L.; Labasi, Jeffrey M.; Zhu, Yucui; Tang, Xiuwei; McClure, Kim; Gabel, Christopher A.; Athar, Mohammad; Bickers, David R.

doi:10.1111/j.0022-202x.2005.23747.x

Cited by 156Skin Protection and AgingProtein Kinase Regulation and GTPase SignalingMelanoma and MAPK Pathways

Role of P38 MAPK in UVB-Induced Inflammatory Responses in the Skin of SKH-1 Hairless Mice

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Kim, Arianna L., Labasi, Jeffrey M., Zhu, Yucui, Tang, Xiuwei, McClure, Kim, Gabel, Christopher A., Athar, Mohammad, Bickers, David R.·2005·Journal of Investigative Dermatology

DOI 10.1111/j.0022-202x.2005.23747.x

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Abstract

The p38 mitogen-activated protein kinase (MAPK) signaling pathway is activated by numerous inflammatory mediators and environmental stresses. We assessed the effects of ultraviolet B (UVB) on the p38 MAPK pathway and determined whether cyclooxygenase (COX)-2 expression is downstream of this kinase in the skin of UVB-irradiated SKH-1 mice. SKH-1 mice were irradiated with a single dose of UVB (360 mJ per cm2), and activation of the epidermal p38 MAPK pathway was assessed. UVB-induced phosphorylation of p38 MAPK occurred in a time-dependent manner. Phosphorylation of MAPK-activated protein kinase-2 (MAPKAPK-2) also was detected and correlated with an increase in its kinase activity. Phosphorylation of heat shock protein 27 (HSP27), a substrate for MAPKAPK-2, also was detected post-irradiation. Oral administration of the p38 inhibitor, SB242235, prior to UVB irradiation, blocked activation of the p38 MAPK cascade, and abolished MAPKAPK-2 kinase activity and phosphorylation of HSP27. Moreover, SB242235 inhibited expression of the pro-inflammatory cytokines interleukin (IL)-6 and KC (murine IL-8) and COX-2. Our data demonstrate that UVB irradiation of murine skin activates epidermal p38 MAPK signaling and induces a local pro-inflammatory response. Blockade of the p38 MAPK pathway may offer an effective approach to reducing or preventing skin damage resulting from acute solar radiation.

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UV radiation promotes inflammation through several distinct mechanisms, such as activation of the inflammasome and pro-inflammatory cytokines, as well as major inflammation-related signaling pathways such as NF-κB and p38.
“UV radiation promotes inflammation through several distinct mechanisms, such as activation of the inflammasome and pro-inflammatory cytokines, as well as major inflammation-related signaling pathways such as NF-κB and p38 ( 34 , 35 )”
From Photorepair of Either CPD or 6-4PP DNA Lesions in Basal Keratinocytes Attenuates Ultraviolet-Induced Skin Effects in Nucleotide Excision Repair Deficient Mice (2022) · cites this paper as [34]
The Discussion reports that UVB activates p38 MAPK, increases pro-inflammatory cytokines, and is known to activate NF-κB in skin cells. Our copy does not address inflammasome activation, so it supports only part of the cited sentence. Page numbers were not available in the indexed passages. (LLM, conf=0.88)
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Authors: Kim, A. L., Labasi, J. M., Zhu, Y., Tang, X., McClure, K., Gabel, C. A., Athar, M., & Bickers, D. R.
Affiliations: Columbia University Irving Medical Center (US)
Pfizer (United States) (US)
Columbia University (US)
Corresponding author: Kim, Arianna L.
ORCID: Kim, Arianna L.
McClure, Kim
Gabel, Christopher A.
Athar, Mohammad
Venue: Journal of Investigative Dermatology
Publisher: Elsevier BV
Published: 2005-06
Volume: 124
Issue: 6
Pages: 1318-1325
ISSN: 0022-202X (ISSN-L)
DOI: 10.1111/j.0022-202x.2005.23747.x
OpenAlex: W1964414267
Cited by: 153
References: 61
Citations by year: 2026: 4 · 2025: 2 · 2024: 12 · 2023: 6 · 2022: 17 · 2021: 10 · 2020: 4 · 2019: 10 · 2018: 8 · 2017: 7 · 2016: 6 · 2015: 6 · 2014: 7 · 2013: 9 · 2012: 8
FWCI: 8.89
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, 3836 d)
Locations: Journal of Investigative Dermatology (publishedVersion)
PubMed (publishedVersion)
Funders: Pfizer
National Institute of Arthritis and Musculoskeletal and Skin Diseases (K01AR048582)
Topics: Health Sciences › Medicine › Dermatology › Skin Protection and Aging
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
Keywords: p38 MAPK, UV-B radiation, skin inflammation, SKH-1 mice, cyclooxygenase-2, MAPKAPK2, HSP27, interleukin-6, photoprotection
MeSH terms: MAP-Kinase-Activated Kinase 2, Animals, Enzyme Inhibitors, Female, Heat-Shock Proteins, Imidazoles, Mice, Hairless, Phosphorylation, Photosensitivity Disorders, Prostaglandin-Endoperoxide Synthases, Pyridines, Skin, Threonine, Ultraviolet Rays, Signal Transduction, Cytokines, Protein Serine-Threonine Kinases, Inflammation Mediators, Intracellular Signaling Peptides and Proteins, p38 Mitogen-Activated Protein Kinases, Mice, Cyclooxygenase 2, HSP27 Heat-Shock Proteins

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Role of P38 MAPK in UVB-Induced Inflammatory Responses in the Skin of SKH-1 Hairless Mice

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