miR-146b level and variants is associated with endometriosis related macrophages phenotype and plays a pivotal role in the endometriotic pain symptom

miR-146b 水平和变异与子宫内膜异位症相关巨噬细胞表型相关,并在子宫内膜异位症疼痛症状中起关键作用

阅读:10
作者:Zengzhen Zhang, Huiqing Li, Zhitao Zhao, Baofeng Gao, Li Meng, Xianguang Feng

Conclusions

Our findings suggest an important role of miR-146b level and variants in endometriosis that helps to regulate the process of endometriosis and its associated pain.

Methods

Genotyping and expression of miR-146b was performed on 74 endometriosis patients and 23 healthy controls. ESCs were subsequently co-cultured with peripheral blood (PB)-derived monocytes (PBMC)-driven macrophages. After overexpression and inhibition of miR-146b, cytokine production from the macrophages were determined by enzyme-linked immunosorbent assay (ELISA). Western blot were done to measure the regulation of IRF5 by miR-146b.

Objective

The aim of this study was to explore the effect of miR-146b expression and variants on endometriosis and its associated pain symptom. Materials and

Results

We found that miR-146b expression was increased in PF supernatant and PF CD14 + monocytes/Macrophages of endometriosis patients, with endometriosis patients with pain (EPWP) showing higher miR-146b expression compared with the endometriosis patients without pain (EPNP). CT/CC genotype of miR-146b rs1536309 was associated with the risk of pain symptom of endometriosis. For the function studies, we found that miR-146b was involved in the negative regulation of inflammation through attenuating IRF5 expression. Macrophages from patients who carries CT/CC genotype of miR-146b rs1536309 showed decreasing miR-146b expression and enhancement of the ability of pro-inflammation. Conclusions: Our findings suggest an important role of miR-146b level and variants in endometriosis that helps to regulate the process of endometriosis and its associated pain.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。