ArticleExperimental dermatology2017
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.
Article in Experimental dermatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Article
- microRNAs involved in psoriasis and cardiovascular diseases.Vascular biology (Bristol, England) · 2021Review
- MicroRNA-17-92 cluster promotes the proliferation and the chemokine production of keratinocytes: implication for the pathogenesis of psoriasis.Cell death & disease · 2018Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
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.
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