Neutrophil-Derived MicroRNA-1290 Promotes Keratinocyte Proliferation in Psoriasis

被引:0
|
作者
Higashi, Yuko [1 ]
Yamakuchi, Munekazu [2 ]
Ibusuki, Atsuko [1 ]
Okubo, Aoi [1 ]
Fukushige, Tomoko [1 ]
Hashiguchi, Teruto [2 ]
Kanekura, Takuro [1 ]
机构
[1] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Dermatol, 8-35-1 Sakuragaoka, Kagoshima 8908520, Japan
[2] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Lab & Vasc Med, 8-35-1 Sakuragaoka, Kagoshima 8908520, Japan
基金
日本学术振兴会;
关键词
psoriasis; neutrophil; microRNA; proliferation; keratinocyte; MYELOID LINEAGE LEUKOCYTES; THERAPEUTIC DEPLETION; BIOMARKERS; EXPRESSION;
D O I
10.1016/j.jid.2023.10.042
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
The pathological hallmark of psoriasis is the infiltration of neutrophils into the skin. Some neutrophil-derived microRNAs (miRNAs) serve as biomarkers for various diseases, but none have been reported for psoriasis. In this study, we investigated the involvement of miRNAs released from neutrophils in psoriasis pathogenesis. We compared the expression of miRNAs in the sera of patients with psoriasis with that in healthy individuals and found that the expression of 2 miRNAs-miR-223 and miR-1290-was significantly upregulated in the sera of patients with psoriasis. The serum levels of these miRNAs positively correlated with the PASI and CRP levels. We used all-trans retinoic acid to induce the differentiation of human promyelocytic leukemia HL-60 cells into neutrophil-like cells and found that the release of both miRNAs increased during differentiation. Furthermore, the release of miR-1290 was increased by TNF-a in neutrophil-like cells and human neutrophils. Treatment with the miR-1290 precursor promoted the proliferation of human keratinocytes, increased the proportion of S-phase cells, and upregulated the phosphorylation of extracellular signal-regulated kinase 1/2. These results suggest that miR-1290 plays a vital role in regulating neutrophil differentiation and keratinocyte proliferation and could be a serum marker of psoriasis severity.
引用
收藏
页码:1471 / 1478.e6
页数:14
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