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miRNA miR-17-92 cluster is differentially regulated in the imiqumod-treated skin but is not required for imiqumod-induced psoriasis-like dermatitis in mice

  • Dinghong Wu
  • , Xinling Bi
  • , Le Qu
  • , Ling Han
  • , Congcong Yin
  • , Jingwen Deng
  • , Zheng Dong
  • , Qing Sheng Mi
  • , Li Zhou

Research output: Contribution to journalLetterpeer-review

Abstract

MicroRNAs (miRNAs) play very important roles in the control of immune cell and keratinocyte development and function and are implicated in skin inflammatory diseases, including psoriasis. miRNA miR-17-92 was reported to promote the differentiation of Th1 and Th1 cells and to regulate cell proliferation and apoptosis. Here we showed that imiquimod (IMQ) differentially regulates the expression of miR-17-92 cluster in the mouse skin, upregulating miR-17 and miR-19 families and downregulating miR-92. To investigate whether miR-17-92 cluster is functionally involved in the psoriasis, we have generated three mutant mice with specific deletion or overexpression of miR-17-92 cluster in keratinocytes, or with deletion of miR-17-92 cluster in T cells. Interestingly, deletion or overexpression of miR-17-92 cluster in keratinocytes, or deletion of miR-17-92 in T cells did not significantly affect IMQ-induced psoriasis-like dermatitis development in the mutant mice compared with wild-type littermates. Thus, miRNA miR-17-92 cluster may not be a key factor regulating imiqumod-induced psoriasis-like dermatitis.

Original languageEnglish (US)
Pages (from-to)82-84
Number of pages3
JournalExperimental Dermatology
Volume26
Issue number1
DOIs
StatePublished - Jan 1 2017

Keywords

  • T cells
  • imiqumod
  • knockin
  • knockout
  • miRNAs
  • psoriasis

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology

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