Li Jiyun, Wu Guimei, Cao Yanmin, Hou Zhi
Third Department of Obstetrical, Hebei Cangzhou Central Hospital, Hebei, China.
Arch Med Sci. 2019 Jan;15(1):183-190. doi: 10.5114/aoms.2018.73129. Epub 2018 Feb 2.
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.
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.
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).
miR-210 can promote proliferation, migration, and invasion via downregulating PTPN2 in the PDGFR-Akt pathway.
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。
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。
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）。
miR-210可通过下调PDGFR-Akt途径中的PTPN2促进增殖、迁移和侵袭。
