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 language | English (US) |
---|---|
Pages (from-to) | 82-84 |
Number of pages | 3 |
Journal | Experimental Dermatology |
Volume | 26 |
Issue number | 1 |
DOIs | |
State | Published - Jan 1 2017 |
Fingerprint
Keywords
- T cells
- imiqumod
- knockin
- knockout
- miRNAs
- psoriasis
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Dermatology
Cite this
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. / Wu, Dinghong; Bi, Xinling; Qu, Le; Han, Ling; Yin, Congcong; Deng, Jingwen; Dong, Zheng; Mi, Qing Sheng; Zhou, Li.
In: Experimental Dermatology, Vol. 26, No. 1, 01.01.2017, p. 82-84.Research output: Contribution to journal › Letter
}
TY - JOUR
T1 - 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
AU - Wu, Dinghong
AU - Bi, Xinling
AU - Qu, Le
AU - Han, Ling
AU - Yin, Congcong
AU - Deng, Jingwen
AU - Dong, Zheng
AU - Mi, Qing Sheng
AU - Zhou, Li
PY - 2017/1/1
Y1 - 2017/1/1
N2 - 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.
AB - 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.
KW - T cells
KW - imiqumod
KW - knockin
KW - knockout
KW - miRNAs
KW - psoriasis
UR - http://www.scopus.com/inward/record.url?scp=85007072201&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85007072201&partnerID=8YFLogxK
U2 - 10.1111/exd.13186
DO - 10.1111/exd.13186
M3 - Letter
C2 - 27579777
AN - SCOPUS:85007072201
VL - 26
SP - 82
EP - 84
JO - Experimental Dermatology
JF - Experimental Dermatology
SN - 0906-6705
IS - 1
ER -