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RPL22 Overexpression Promotes Psoriasis-Like Lesion by Inducing Keratinocytes Abnormal Biological Behavior

BACKGROUND: Keratinocytes of psoriasis have anti-apoptotic properties including delayed apoptosis process, accelerated proliferation metabolism and postponed differentiation process. However, the specific mechanism leading to the abnormal biological behavior of keratinocytes remains unclear. OBJECTI...

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Autores principales: Zeng, Jinrong, Zhang, Yue, Zhang, Hanyi, Zhang, Yuezhong, Gao, Lihua, Tong, Xiaoliang, Xie, Yajie, Hu, Qian, Chen, Chunli, Ding, Shu, Lu, Jianyun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8250439/
https://www.ncbi.nlm.nih.gov/pubmed/34220863
http://dx.doi.org/10.3389/fimmu.2021.699900
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author Zeng, Jinrong
Zhang, Yue
Zhang, Hanyi
Zhang, Yuezhong
Gao, Lihua
Tong, Xiaoliang
Xie, Yajie
Hu, Qian
Chen, Chunli
Ding, Shu
Lu, Jianyun
author_facet Zeng, Jinrong
Zhang, Yue
Zhang, Hanyi
Zhang, Yuezhong
Gao, Lihua
Tong, Xiaoliang
Xie, Yajie
Hu, Qian
Chen, Chunli
Ding, Shu
Lu, Jianyun
author_sort Zeng, Jinrong
collection PubMed
description BACKGROUND: Keratinocytes of psoriasis have anti-apoptotic properties including delayed apoptosis process, accelerated proliferation metabolism and postponed differentiation process. However, the specific mechanism leading to the abnormal biological behavior of keratinocytes remains unclear. OBJECTIVES: We investigated the role of increased RPL22 expression in regulating the abnormal biological behavior of keratinocytes and the mechanism of regulation of RPL22 expression in skin lesions of psoriatic patients. METHODS: We examined clinical samples and utilized cytokine-induced cell and IMQ-treated mouse models. We determined the expression and functions of RPL22 in vitro and in vivo. RESULTS: We showed that RPL22 expression was significantly increased in the skin lesions of psoriasis patients and IMQ-treated psoriatic-like mice. Such increased expression is attributed to hyperacetylation of histone H3K27 in the promoter region of RPL22. Interestingly, overexpression of RPL22 enhanced keratinocyte proliferation by increasing cyclinD1 expression and accelerated CD4(+)T cells recruitment via upregulating CXCL10 expression. Finally, we demonstrated that RPL22 overexpression promoted psoriasiform phenotypes in IMQ-induced mouse skins. CONCLUSIONS: These findings suggested that RPL22 regulates keratinocytes abnormal biological behavior and contributes to the development of psoriatic phenotypes. Thus, RPL22 might be a novel potential molecular target for treatment of psoriasis.
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spelling pubmed-82504392021-07-03 RPL22 Overexpression Promotes Psoriasis-Like Lesion by Inducing Keratinocytes Abnormal Biological Behavior Zeng, Jinrong Zhang, Yue Zhang, Hanyi Zhang, Yuezhong Gao, Lihua Tong, Xiaoliang Xie, Yajie Hu, Qian Chen, Chunli Ding, Shu Lu, Jianyun Front Immunol Immunology BACKGROUND: Keratinocytes of psoriasis have anti-apoptotic properties including delayed apoptosis process, accelerated proliferation metabolism and postponed differentiation process. However, the specific mechanism leading to the abnormal biological behavior of keratinocytes remains unclear. OBJECTIVES: We investigated the role of increased RPL22 expression in regulating the abnormal biological behavior of keratinocytes and the mechanism of regulation of RPL22 expression in skin lesions of psoriatic patients. METHODS: We examined clinical samples and utilized cytokine-induced cell and IMQ-treated mouse models. We determined the expression and functions of RPL22 in vitro and in vivo. RESULTS: We showed that RPL22 expression was significantly increased in the skin lesions of psoriasis patients and IMQ-treated psoriatic-like mice. Such increased expression is attributed to hyperacetylation of histone H3K27 in the promoter region of RPL22. Interestingly, overexpression of RPL22 enhanced keratinocyte proliferation by increasing cyclinD1 expression and accelerated CD4(+)T cells recruitment via upregulating CXCL10 expression. Finally, we demonstrated that RPL22 overexpression promoted psoriasiform phenotypes in IMQ-induced mouse skins. CONCLUSIONS: These findings suggested that RPL22 regulates keratinocytes abnormal biological behavior and contributes to the development of psoriatic phenotypes. Thus, RPL22 might be a novel potential molecular target for treatment of psoriasis. Frontiers Media S.A. 2021-06-18 /pmc/articles/PMC8250439/ /pubmed/34220863 http://dx.doi.org/10.3389/fimmu.2021.699900 Text en Copyright © 2021 Zeng, Zhang, Zhang, Zhang, Gao, Tong, Xie, Hu, Chen, Ding and Lu https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Zeng, Jinrong
Zhang, Yue
Zhang, Hanyi
Zhang, Yuezhong
Gao, Lihua
Tong, Xiaoliang
Xie, Yajie
Hu, Qian
Chen, Chunli
Ding, Shu
Lu, Jianyun
RPL22 Overexpression Promotes Psoriasis-Like Lesion by Inducing Keratinocytes Abnormal Biological Behavior
title RPL22 Overexpression Promotes Psoriasis-Like Lesion by Inducing Keratinocytes Abnormal Biological Behavior
title_full RPL22 Overexpression Promotes Psoriasis-Like Lesion by Inducing Keratinocytes Abnormal Biological Behavior
title_fullStr RPL22 Overexpression Promotes Psoriasis-Like Lesion by Inducing Keratinocytes Abnormal Biological Behavior
title_full_unstemmed RPL22 Overexpression Promotes Psoriasis-Like Lesion by Inducing Keratinocytes Abnormal Biological Behavior
title_short RPL22 Overexpression Promotes Psoriasis-Like Lesion by Inducing Keratinocytes Abnormal Biological Behavior
title_sort rpl22 overexpression promotes psoriasis-like lesion by inducing keratinocytes abnormal biological behavior
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8250439/
https://www.ncbi.nlm.nih.gov/pubmed/34220863
http://dx.doi.org/10.3389/fimmu.2021.699900
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