LncRNA H19 over-expression inhibited Th17 cell differentiation to relieve endometriosis through miR-342-3p/IER3 pathway

Zheying Liu,Chaoyue Tan,Yun Zhong,Junbi Gao,Mingbo Cai,Liping Han,Xiaoxiao Han,Ruixia Guo,Liya Liu

doi:10.1186/s13578-019-0346-3

Zheying Liu, Chaoyue Tan + Show 7 more

Open Access

https://doi.org/10.1186/s13578-019-0346-3

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Abstract

ObjectiveTo investigate the mechanism of LncRNA H19 in Th17 cell differentiation and endometrial stromal cells (ESCs) proliferation in endometriosis (EMS).MethodsLncRNA H19, miR-342-3p and IER3 expressions were detected by qRT-PCR and western blot. The percentage of Th17 cells/CD4+ T cells was detected by flow cytometry. IL-17 level was measured by ELISA. The interaction of miR-342-3p and IER3 was confirmed by Luciferase reporter assay.ResultsLncRNA H19 and IER3 expressions were down-regulated in mononuclear cells from peritoneal fluid (PFMCs) of patients with EMS or under Th17 differentiation conditions, whereas miR-342-3p expression was up-regulated and the percentage of Th17 cells was increased in PFMCs of patients with EMS or under Th17 differentiation conditions. Over-expression of LncRNA H19 decreased IL-17 level and the percentage of Th17 cells/CD4+ T cells. Besides, we confirmed that miR-342-3p could target to IER3 and negatively regulate IER3 expression. LncRNA H19 over-expression suppressed Th17 differentiation and ESC proliferation through regulating miR-342-3p/IER3. In vivo experiments showed LncRNA H19 over-expression suppressed the growth of Th17 cell differentiation-induced endometriosis-like lesions.ConclusionLncRNA H19 was down-regulated in PFMC of patients with EMS or under Th17 polarizing conditions, and LncRNA H19 over-expression suppressed Th17 cell differentiation and ESCs proliferation through miR-342-3p/IER3 pathway.

Highlights

Endometriosis (EMS) is a common gynecological disorder characterized by the presence of endometrial tissue outside the uterine cavity, which affects approximately 10% of reproductive-aged women and causes pain and infertility [1]
We showed that LncRNA H19 was downregulated in mononuclear cells from peritoneal fluid (PFMCs) of patients with EMS, and found over-expression of H19 decreased the secretion of IL-17 and reduced the percentage of T helper cell 17 (Th17) cells/CD4+ T cells through miR342-3p/IER3, thereby contributing to suppress Th17 differentiation and endometrial stromal cells (ESCs) proliferation
LncRNA H19 was down‐regulated in PFMC of patients with EMS We first examined the expressions of LncRNA H19, miR-342-3p and IER3 in PFMCs in patients with EMS

Summary

Introduction

Endometriosis (EMS) is a common gynecological disorder characterized by the presence of endometrial tissue outside the uterine cavity, which affects approximately 10% of reproductive-aged women and causes pain and infertility [1]. This disease has been investigated for decades, the pathogenesis of EMS is still not fully understood. We assume that IER3 might involve in the signaling pathways that regulate Th17 cells in EMS. Bioinformatics software predicts IER3 is one of the target genes of miR342-3p. MiR-342-3p may involve in the regulation of Th17 cells in EMS through targeting IER3

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