2016
DOI: 10.1038/srep19588
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Hypoxia-inducible miR-210 contributes to preeclampsia via targeting thrombospondin type I domain containing 7A

Abstract: Preeclampsia, a relatively common pregnancy disorder, is a major contributor to maternal mortality and morbidity worldwide. An elevation in microRNA-210 (miR-210) expression in the placenta has been reported to be associated with preeclampsia. Our bioinformatic analysis showed that thrombospondin type I domain containing 7A (THSD7A) is a predicted target for miR-210. The aim of this study was to determine whether miR-210 is involved in preeclampsia through its targeting of THSD7A in human placental trophoblast… Show more

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Cited by 84 publications
(62 citation statements)
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“…miR-210 has also been associated with hypoxia in placental trophoblasts and shown to be upregulated in diseases attributed to hypoxia, such as preeclampsia, [9, 10]. Luo et al [11] provide evidence that miR-210 downregulates Thrombospondin Type I Domain Containing 7A (THSD7A) in human placental trophoblasts, possibly contributing to the preeclamptic phenotype. Low oxygen tension also leads to placental mitochondria dysfunction, in which elevated miR-210 levels downregulate the Iron Sulfur Cluster (ISCU) gene and inhibition of miR-210 protects trophoblast cells form oxidative stress [12].…”
Section: Introductionmentioning
confidence: 99%
“…miR-210 has also been associated with hypoxia in placental trophoblasts and shown to be upregulated in diseases attributed to hypoxia, such as preeclampsia, [9, 10]. Luo et al [11] provide evidence that miR-210 downregulates Thrombospondin Type I Domain Containing 7A (THSD7A) in human placental trophoblasts, possibly contributing to the preeclamptic phenotype. Low oxygen tension also leads to placental mitochondria dysfunction, in which elevated miR-210 levels downregulate the Iron Sulfur Cluster (ISCU) gene and inhibition of miR-210 protects trophoblast cells form oxidative stress [12].…”
Section: Introductionmentioning
confidence: 99%
“…A great number of differentially expressed miRNAs have been identified in preeclamptic placentas, [15][16][17] and some of these differentially expressed miRNAs were demonstrated to participate in the regulation of various placental cell events and functions. [18][19][20] On the basis of these data, we speculate that the abnormally elevated androgen in PE patients may upregulate miR-22 expression in placental trophoblasts, which may target and repress ERα and aromatase and, accordingly, exacerbate the imbalanced production of androgen and estrogen in patients.To address this assumption, we examined the differential production of miR-22, 17β-HSD3, and aromatase in severe PE placentas. The effects of testosterone on miR-22, aromatase, and ERα expression, as well as estradiol production, were explored in the human trophoblastic cell line JEG-3.…”
mentioning
confidence: 99%
“…There are five main oxidative stress cell models used to investigate pregnancy complications (11)(12)(13)(14)(15). Firstly, there is hypoxia or low partial pressure of oxygen (<5% o 2 ) (13,16,17). researchers usually culture cells in 1-2% o 2 for 12-72 h as a hypoxic condition to induce oxidative stress (13,16,17).…”
Section: Introductionmentioning
confidence: 99%
“…Firstly, there is hypoxia or low partial pressure of oxygen (<5% o 2 ) (13,16,17). researchers usually culture cells in 1-2% o 2 for 12-72 h as a hypoxic condition to induce oxidative stress (13,16,17). Hypoxia is perceived as the oxidative stress model for pregnancy complications because trophoblast invasion and/or vascular remodeling are compromised (18).…”
Section: Introductionmentioning
confidence: 99%