Skip to search boxSkip to navigationSkip to main content

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
*Corresponding author for this work
  • Henry Ford Health System
    ,
  • Guangdong Provincial Hospital of Traditional Chinese Medicine
    ,
  • ,
  • Wayne State University
Scholary Output:
Contribution to journal
Letter
Peer-review

Open access

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.

Publication Information

Output type

Scholary Output:
Contribution to journal
Letter
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 82-84 (3 pages)

Journal (Volume, Issue Number)

Experimental Dermatology (Volume 26, Issue 1)

Publication milestones

  • Published - 01/01/2017

Publication status

Published - 01/01/2017

ISSN

0906-6705

Publication IDs

  • Scopus: 85007072201
  • PubMed: 27579777

Publication metrics

Metrics

SciVal
citations
4
Scopus
citations
SciVal
FWCI
0.61
SciVal
Author count
9
SciVal
Paper percentile
56
Fractional count
1
Fractional count
0.11
Fractional count
8
Fractional count
0.89
Fractional count
1
Fractional count
1

PlumX, opens in new tab

Citation count
7
Captures
11

Funding Details

This work was supported in part by grant from Guangdong Science and Technology Department Program 2013B0021800237 to WD, NIH Grant R21AR059976, 1R56AI119041-01, 1R01AR069681-01 and 1R01AI119041-01A1 to MQS and Henry Ford Health System Immunology Program Start-up Grant T71017 to ZL.
FundersFunding numbers
Guangdong Science and Technology Department Program
2013B0021800237
NIH
1R56AI119041-01, R21AR059976, T71017
NIAMS
R01AR069681