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Overexpression of Lin28a Aggravates Psoriasis-Like Phenotype by Regulating the Proliferation and Differentiation of Keratinocytes.
Jang, Soyeon; Jang, Soyoung; Kim, Si-Yong; Ko, Jiwon; Kim, Eungyung; Park, Ji Yeong; Hyung, Hyejin; Lee, Jin Hong; Lim, Su-Geun; Park, Sijun; Yi, Junkoo; Lee, Heon-Jin; Kim, Myoung Ok; Lee, Hyun-Shik; Ryoo, Zae Young.
Afiliación
  • Jang S; School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, Korea.
  • Jang S; School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, Korea.
  • Kim SY; School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, Korea.
  • Ko J; School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, Korea.
  • Kim E; Department of Animal Science and Biotechnology, Kyungpook National University, Daegu, Korea.
  • Park JY; School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, Korea.
  • Hyung H; School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, Korea.
  • Lee JH; School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, Korea.
  • Lim SG; School of Life Science, Kyungpook National University, Daegu, Korea.
  • Park S; School of Life Science, Kyungpook National University, Daegu, Korea.
  • Yi J; Gyeongsangbukdo Livestock Research Institute, Yeongju, Korea.
  • Lee HJ; Department of Microbiology and Immunology, School of Dentistry, Kyungpook National University, Daegu, 41940, Korea.
  • Kim MO; Department of Animal Science and Biotechnology, Kyungpook National University, Daegu, Korea.
  • Lee HS; School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, Korea.
  • Ryoo ZY; School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, Korea.
J Inflamm Res ; 14: 4299-4312, 2021.
Article en En | MEDLINE | ID: mdl-34511969
PURPOSE: Psoriasis is a common and well-studied autoimmune skin disease, which is characterized by plaques. The formation of psoriasis plaques occurs through the hyperproliferation and abnormal differentiation of keratinocytes, infiltration of numerous immune cells into the dermis, increased subepidermal angiogenesis, and various autoimmune-associated cytokines and chemokines. According to previous research, Lin28 regulates the let-7 family, and let-7b is associated with psoriasis. However, the link between Lin28 and psoriasis is unclear. In this study, an association was identified between Lin28a and psoriasis progression, which promoted the pathological characteristic of psoriasis in epidermal keratinocytes. PATIENTS AND METHODS: This study aims to investigate the role of Lin28a and its underlying mechanism in psoriasis through in vivo and in vitro models, which include the Lin28a-overexpressing transgenic (TG) mice and Lin28a-overexpressing human keratinocyte (HaCaT) cell lines, respectively. RESULTS: In vivo and in vitro results revealed that overexpression of Lin28a downregulated microRNA let-7 expression levels and caused hyperproliferation and abnormal differentiation in keratinocytes. In imiquimod (IMQ)-induced psoriasis-like inflammation, Lin28a overexpressing transgenic (TG) mice exhibited more severe symptoms of psoriasis. CONCLUSION: Mechanistically, Lin28a exacerbated psoriasis-like inflammation through the activation of the extracellular-signal-regulated kinase (ERK) and signal transducer and activator of transcription 3 signaling (STAT 3) by targeting proinflammatory cytokine interleukin-6 (IL-6).
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: J Inflamm Res Año: 2021 Tipo del documento: Article Pais de publicación: Nueva Zelanda

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: J Inflamm Res Año: 2021 Tipo del documento: Article Pais de publicación: Nueva Zelanda