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微小RNA-210在子痫前期发病机制中的作用。

Roles of miR-210 in the pathogenesis of pre-eclampsia.

作者信息

Li Jiyun, Wu Guimei, Cao Yanmin, Hou Zhi

机构信息

Third Department of Obstetrical, Hebei Cangzhou Central Hospital, Hebei, China.

出版信息

Arch Med Sci. 2019 Jan;15(1):183-190. doi: 10.5114/aoms.2018.73129. Epub 2018 Feb 2.

Abstract

INTRODUCTION

This study aimed to explore the bio-function of miR-210 in the pathogenesis of pre-eclampsia and provide new insights into the diagnosis and treatment of pre-eclampsia.

MATERIAL AND METHODS

A JAR cell line cultured in standard or hypoxic conditions was used in this study. Expression levels of miR-210 and PTPN2 were determined using real-time polymerase chain reaction (RT-PCR). Protein and phosphorylation levels were assessed using western blotting. Proliferation of JAR cells was evaluated using MTT assay. Migration and invasion were measured using transwell assay.

RESULTS

Expression of miR-210 increased significantly in a time-dependent manner after hypoxia treatment within 36 h ( < 0.05). miR-210 inhibitor significantly decreased the cell proliferation, migration, and invasion ( < 0.05), while miR-210 mimic reversed these findings ( < 0.05). Hypoxia significantly suppressed the expression of PTPN2; however, this elevation was abolished by miR-210 inhibitor ( < 0.05). Inhibition of PTPN2 or hypoxia significantly increased the proliferation, migration, and invasion of JAR cells, while miR-210 inhibitor significantly reversed these changes ( < 0.05). The phosphorylation levels of PDGFR, Akt, and Erk were markedly upregulated by hypoxia or si-PTPN2, but this effect was abolished by miR-210 inhibitor ( < 0.05).

CONCLUSIONS

miR-210 can promote proliferation, migration, and invasion via downregulating PTPN2 in the PDGFR-Akt pathway.

摘要

引言

本研究旨在探讨miR-210在子痫前期发病机制中的生物学功能,并为子痫前期的诊断和治疗提供新的见解。

材料与方法

本研究使用在标准或缺氧条件下培养的JAR细胞系。采用实时聚合酶链反应(RT-PCR)测定miR-210和PTPN2的表达水平。使用蛋白质印迹法评估蛋白质和磷酸化水平。采用MTT法评估JAR细胞的增殖情况。使用Transwell法测量迁移和侵袭能力。

结果

缺氧处理36小时内,miR-210的表达呈时间依赖性显著增加(<0.05)。miR-210抑制剂显著降低细胞增殖、迁移和侵袭能力(<0.05),而miR-210模拟物则逆转了这些结果(<0.05)。缺氧显著抑制PTPN2的表达;然而,miR-210抑制剂消除了这种升高(<0.05)。抑制PTPN2或缺氧显著增加JAR细胞的增殖、迁移和侵袭能力,而miR-210抑制剂显著逆转了这些变化(<0.05)。缺氧或si-PTPN2显著上调PDGFR、Akt和Erk的磷酸化水平,但miR-210抑制剂消除了这种作用(<0.05)。

结论

miR-210可通过下调PDGFR-Akt途径中的PTPN2促进增殖、迁移和侵袭。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f35/6348360/b8fc8d0dc09e/AMS-15-31622-g001.jpg

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