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SERPINB4 Promotes Keratinocyte Inflammation via p38MAPK Signaling Pathway

Psoriasis is a chronic inflammatory skin disease characterized by infiltration of inflammatory cells and excessive proliferation of epidermal keratinocytes. SERPINB4, as a serine protease inhibitor, has been clearly expressed in the skin lesions and serum of patients with psoriasis, but the specific...

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Detalles Bibliográficos
Autores principales: Zhang, Yanan, Wang, Luling, Sun, Xiaoying, Li, Fulun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10049849/
https://www.ncbi.nlm.nih.gov/pubmed/36999136
http://dx.doi.org/10.1155/2023/3397940
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author Zhang, Yanan
Wang, Luling
Sun, Xiaoying
Li, Fulun
author_facet Zhang, Yanan
Wang, Luling
Sun, Xiaoying
Li, Fulun
author_sort Zhang, Yanan
collection PubMed
description Psoriasis is a chronic inflammatory skin disease characterized by infiltration of inflammatory cells and excessive proliferation of epidermal keratinocytes. SERPINB4, as a serine protease inhibitor, has been clearly expressed in the skin lesions and serum of patients with psoriasis, but the specific mechanism of action is not yet clear. Here, we showed that SERPINB4 expression was increased in skin lesions from the imiquimod (IMQ)-treated mice and M5-(a mixture of five proinflammatory cytokines: IL-17A, IL-22, IL-1α, oncostatin M, and TNF-α) treated human immortalized keratinocyte (HaCaT). Knockdown of SERPINB4 by short hairpin RNA attenuated the M5-induced keratinocyte inflammation. Conversely, lentiviral expression of SERPINB4 promoted keratinocyte inflammation. Finally, we observed that SERPINB4 stimulation activated the p38MAPK signaling pathway. Taken together, these results suggest that SERPINB4 has a critical role in psoriasis pathogenesis.
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spelling pubmed-100498492023-03-29 SERPINB4 Promotes Keratinocyte Inflammation via p38MAPK Signaling Pathway Zhang, Yanan Wang, Luling Sun, Xiaoying Li, Fulun J Immunol Res Research Article Psoriasis is a chronic inflammatory skin disease characterized by infiltration of inflammatory cells and excessive proliferation of epidermal keratinocytes. SERPINB4, as a serine protease inhibitor, has been clearly expressed in the skin lesions and serum of patients with psoriasis, but the specific mechanism of action is not yet clear. Here, we showed that SERPINB4 expression was increased in skin lesions from the imiquimod (IMQ)-treated mice and M5-(a mixture of five proinflammatory cytokines: IL-17A, IL-22, IL-1α, oncostatin M, and TNF-α) treated human immortalized keratinocyte (HaCaT). Knockdown of SERPINB4 by short hairpin RNA attenuated the M5-induced keratinocyte inflammation. Conversely, lentiviral expression of SERPINB4 promoted keratinocyte inflammation. Finally, we observed that SERPINB4 stimulation activated the p38MAPK signaling pathway. Taken together, these results suggest that SERPINB4 has a critical role in psoriasis pathogenesis. Hindawi 2023-03-21 /pmc/articles/PMC10049849/ /pubmed/36999136 http://dx.doi.org/10.1155/2023/3397940 Text en Copyright © 2023 Yanan Zhang et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Zhang, Yanan
Wang, Luling
Sun, Xiaoying
Li, Fulun
SERPINB4 Promotes Keratinocyte Inflammation via p38MAPK Signaling Pathway
title SERPINB4 Promotes Keratinocyte Inflammation via p38MAPK Signaling Pathway
title_full SERPINB4 Promotes Keratinocyte Inflammation via p38MAPK Signaling Pathway
title_fullStr SERPINB4 Promotes Keratinocyte Inflammation via p38MAPK Signaling Pathway
title_full_unstemmed SERPINB4 Promotes Keratinocyte Inflammation via p38MAPK Signaling Pathway
title_short SERPINB4 Promotes Keratinocyte Inflammation via p38MAPK Signaling Pathway
title_sort serpinb4 promotes keratinocyte inflammation via p38mapk signaling pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10049849/
https://www.ncbi.nlm.nih.gov/pubmed/36999136
http://dx.doi.org/10.1155/2023/3397940
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