Roles of miR-210 in the pathogenesis of pre-eclampsia
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 le...
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Autores principales: | , , , |
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Formato: | article |
Lenguaje: | EN |
Publicado: |
Termedia Publishing House
2018
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Materias: | |
Acceso en línea: | https://doaj.org/article/fda2905d4f3d4946b33d00018615042d |
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Sumario: | 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 (p < 0.05). miR-210 inhibitor significantly decreased the cell proliferation, migration, and invasion (p < 0.05), while miR-210 mimic reversed these findings (p < 0.05). Hypoxia significantly suppressed the expression of PTPN2; however, this elevation was abolished by miR-210 inhibitor (p < 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 (p < 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 (p < 0.05).
Conclusions
miR-210 can promote proliferation, migration, and invasion via downregulating PTPN2 in the PDGFR-Akt pathway |
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