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p38α deficiency ameliorates psoriasis development by downregulating STAT3-mediated keratinocyte proliferation and cytokine production.
Zheng, Tingting; Deng, Jiaqi; Wen, Jiahong; Xiao, Shuxiu; Huang, Haiyong; Shang, Jiawen; Zhang, Luwen; Chen, Huan; Li, Jingyu; Wang, Yanyan; Ouyang, Suidong; Yang, Meng; Otsu, Kinya; Liu, Xinguang; Huang, Gonghua.
Afiliación
  • Zheng T; Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China. ting616119@163.com.
  • Deng J; Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China.
  • Wen J; Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China.
  • Xiao S; Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • Huang H; Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China.
  • Shang J; Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China.
  • Zhang L; Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China.
  • Chen H; Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China.
  • Li J; Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China.
  • Wang Y; Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China.
  • Ouyang S; Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China.
  • Yang M; Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China.
  • Otsu K; Department of Cardiovascular Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
  • Liu X; Cardiovascular Division, King's College London, London, UK.
  • Huang G; Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Institute of Aging Research, Institute of Biochemistry & Molecular Biology, Guangdong Medical University, Dongguan, China.
Commun Biol ; 7(1): 999, 2024 Aug 15.
Article en En | MEDLINE | ID: mdl-39147860
ABSTRACT
Psoriasis is characterized by keratinocyte (KC) hyperproliferation and inflammatory cell infiltration, but the mechanisms remain unclear. In an imiquimod-induced mouse psoriasiform model, p38 activity is significantly elevated in KCs and p38α specific deletion in KCs ameliorates skin inflammation. p38α signaling promotes KC proliferation and psoriasis-related proinflammatory gene expression during psoriasis development. Mechanistically, p38α enhances KC proliferation and production of inflammatory cytokines and chemokines by activating STAT3. While p38α signaling in KCs does not affect the expression of IL-23 and IL-17, it substantially amplifies the IL-23/IL-17 pathogenic axis in psoriasis. The therapeutic effect of IL-17 neutralization is associated with decreased p38 and STAT3 activities in KCs and targeting the p38α-STAT3 axis in KCs ameliorates the severity of psoriasis. As IL-17 also highly activates p38 and STAT3 in KCs, our findings reveal a sustained signaling circuit important for psoriasis development, highlighting p38α-STAT3 axis as an important target for psoriasis treatment.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Psoriasis / Queratinocitos / Citocinas / Proteína Quinasa 14 Activada por Mitógenos / Proliferación Celular / Factor de Transcripción STAT3 Límite: Animals / Humans Idioma: En Revista: Commun Biol Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Psoriasis / Queratinocitos / Citocinas / Proteína Quinasa 14 Activada por Mitógenos / Proliferación Celular / Factor de Transcripción STAT3 Límite: Animals / Humans Idioma: En Revista: Commun Biol Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido