MicroRNA-223 Suppresses the Canonical NF-κB Pathway in Basal Keratinocytes to Dampen Neutrophilic Inflammation.
MicroRNA-223 Suppresses the Canonical NF-κB Pathway in Basal Keratinocytes to Dampen Neutrophilic Inflammation.
复制标题
MicroRNA-223抑制基底角质形成细胞中的典型NF-κB通路以抑制嗜中性粒细胞炎症。
DOI：
10.1016/j.celrep.2018.01.058
复制
发表时间：
2018-02-13
期刊：
影响因子：
8.8
通讯作者：
Deng Q
中科院分区：
文献类型：
--
作者：
Zhou W;Pal AS;Hsu AY;Gurol T;Zhu X;Wirbisky-Hershberger SE;Freeman JL;Kasinski AL;Deng Q
MicroRNA-223 is known as a myeloid-enriched anti-inflammatory microRNA that is dysregulated in numerous inflammatory conditions. Here, we report that neutrophilic inflammation (wound response) is augmented in miR-223-deficient zebrafish, due primarily to elevated activation of the canonical nuclear factor κB (NF-κB) pathway. NF-κB over-activation is restricted to the basal layer of the surface epithelium, although miR-223 is detected throughout the epithelium and in phagocytes. Not only phagocytes but also epithelial cells are involved in miR-223-mediated regulation of neutrophils’ wound response and NF-κB activation. Cul1a/b, Traf6, and Tab1 are identified as direct targets of miR-223, and their levels rise in injured epithelium lacking miR-223. In addition, miR-223 is expressed in cultured human bronchial epithelial cells, where it also downregulates NF-κB signaling. Together, this direct connection between miR-223 and the canonical NF-κB pathway provides a mechanistic understanding of the multifaceted role of miR-223 and highlights the relevance of epithelial cells in dampening neutrophil activation. microRNA-223 is dysregulated in many inflammatory conditions such as cancer and asthma, yet its physiological role is not clear. Zhou et al. demonstrate that microRNA-223 in both phagocytes and epithelial cells cooperate to suppress the canonical NF-κB pathway in epithelial cells to restrict the magnitude of inflammation.
登录
查看更多内容
影响因子：
64.8
作者：
Baek, Daehyun;Villen, Judit;Shin, Chanseok;Camargo, Fernando D.;Gygi, Steven P.;Bartel, David P.
通讯作者：
Bartel, David P.
影响因子：
15.9
作者：
Dorhoi, Anca;Iannaccone, Marco;Kaufmann, Stefan H. E.
通讯作者：
Kaufmann, Stefan H. E.
影响因子：
64.8
作者：
Johnnidis, Jonathan B.;Harris, Marian H.;Camargo, Fernando D.
通讯作者：
Camargo, Fernando D.
影响因子：
9.8
作者：
John B;Enright AJ;Aravin A;Tuschl T;Sander C;Marks DS
通讯作者：
Marks DS
DOI：
10.1016/j.urolonc.2007.01.019
发表时间：
2007-09-01
影响因子：
2.7
作者：
Gottardo, Fedra;Liu, Chang Gong;Baffa, Raffaele
通讯作者：
Baffa, Raffaele