Hydrogen sulfide upregulates miR-16-5p targeting PiK3R1 and RAF1 to inhibit neutrophil extracellular trap formation in chickens

文献类型： 外文期刊

第一作者： Yin, Kai

作者： Yin, Kai;Zhang, Hongfu;Yin, Kai;Cui, Yuan;Qu, Yingying;Zhang, Jinxi;Lin, Hongjin;Zhang, Hongfu;Lin, Hongjin

作者机构：

关键词： Hydrogen sulfide (H2S); Neutrophil extracellular traps (NETs); miR-16-5p; Oxidative burst; Ca2+; Autophagy

期刊名称：ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY （ 影响因子：6.291； 五年影响因子：6.393 ）

ISSN： 0147-6513

年卷期： 2020 年 194 卷

页码：

收录情况： SCI

摘要： Hydrogen sulfide (H2S) is a toxic air pollutant that causes immune damage. Recent studies have found that neutrophil extracellular trap (NET) formation is one way in which neutrophils exert immune functions. In addition, the formation of NETs is also related to thrombosis and autoimmune diseases. Recent studies have shown that miRNAs are involved in the regulation of a variety of pathophysiological processes. Here, we investigated the role of H2S in regulating the formation of NETs by affecting miR-16-5p. Our study established an in vitro H2S exposure model for neutrophils using phorbol-myristate-acetate (PMA) to induce NET formation. We observed the morphological changes of cells with scanning electron microscopy and fluorescence microscopy. Then, the content of extracellular DNA and the expression of MPO and NE in each group were detected. The results showed that H2S inhibited the formation of NETs. The expression of miR-16-5p and its target genes PiK3R1 and RAF1 was then measured by qRT-PCR. H2S upregulated miR-16-5p and inhibited expression of the target genes PiK3R1 and RAF1, and it subsequently inhibited the Pi3K/AKT and ERK pathways and decreased respiratory burst levels. Furthermore, H2S attenuated inositol 1,4,5-trisphosphate receptor (IP3R)-mediated endoplasmic reticulum calcium outflow as well as autophagy caused by PMA. This study enriches H2S immunotoxicity research and provides a possible solution for the treatment of NET-related diseases.

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