Elevated levels of hypoxia‐inducible microRNA‐210 in pre‐eclampsia: new insights into molecular mechanisms for the disease

Zhang, Yi; Fei, Mingyu; Geng, Xue; Zhou, Qi; Yin, Jianfei; Li, Li; Xin, Hong; Sun, Shuhan

doi:10.1111/j.1582-4934.2011.01291.x

Cited by 206 publications

(233 citation statements)

References 47 publications

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“…miR-210 was found to be upregulated in trophoblast cells cultured under hypoxic conditions, and in pre-eclamptic patients as compared to healthy controls. 91,100 Interestingly, another study found that miR-210 expression under hypoxia can be regulated by the p50 transcription factor, which in turn regulates HIF-1a in the trophoblast cells. 91 Therefore, miRNAs share regulatory pathways with other placental genes that are altered in pre-eclampsia.…”

Section: Microrna Regulation In the Placentamentioning

confidence: 99%

“…91,100 Interestingly, another study found that miR-210 expression under hypoxia can be regulated by the p50 transcription factor, which in turn regulates HIF-1a in the trophoblast cells. 91 Therefore, miRNAs share regulatory pathways with other placental genes that are altered in pre-eclampsia. 91 In addition to miR-210, other important miRNAs including the miR-17-92 family, which is involved in angiogenesis 101,102 and immune cell development, 103 miR-93, miR-205, miR-335, miR-224, miR-424, miR-451 and miR-491 have been found to be differentially expressed in primary human trophoblasts that were exposed to hypoxia.…”

Section: Microrna Regulation In the Placentamentioning

confidence: 99%

“…104 This is further supported by the fact that miRNAs have multiple roles and share regulatory pathways in the placenta. 91,104 The involvement of miRNAs in human trophoblast differentiation was demonstrated recently when the members of the miR-17-92 cluster as well as the miR-106a-363 family, which are regulated by c-myc oncoprotein, were found to inhibit trophoblast differentiation via repression of aromatase (hCYP19A1) and the transcription factor responsible for murine labyrinthine trophoblast development (human GCM1 or hGCM1). 105 Another miRNA, miR-29b, that appears to have a similar role to the miR-17-92 cluster, has also been implicated in pre-eclampsia.…”

Section: Microrna Regulation In the Placentamentioning

confidence: 99%

“…91 Therefore, miRNAs share regulatory pathways with other placental genes that are altered in pre-eclampsia. 91 In addition to miR-210, other important miRNAs including the miR-17-92 family, which is involved in angiogenesis 101,102 and immune cell development, 103 miR-93, miR-205, miR-335, miR-224, miR-424, miR-451 and miR-491 have been found to be differentially expressed in primary human trophoblasts that were exposed to hypoxia. 104 Additionally, miR-205 has been found to be linked to placental development in humans.…”

Section: Microrna Regulation In the Placentamentioning

confidence: 99%

“…These include fetal weight restriction and low fetal birth weight (intrauterine growth retardation or IUGR), [81][82][83][84] toxin exposures such as environmental toxins, 85,86 cancer (hepatocellular carcinoma), 87 diabetes mellitus 88 and, the most heavily studied, human pre-eclampsia. 79,[89][90][91][92][93][94][95][96] Many of the pre-eclampsia studies have investigated miRNA expression using high throughput microarray, and qPCR (primarily in order to validate specific microarray findings). Previous studies have established that oxygen tension is implicated in placental development in humans and mice.…”

Section: Microrna Regulation In the Placentamentioning

confidence: 99%

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MicroRNAs, immune cells and pregnancy

et al. 2014

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MicroRNAs (miRNAs) are a recently discovered class of non-coding RNAs that are expressed in many cell types, where they regulate the expression of complementary RNAs, thus modulating the stability and translation of mRNAs. miRNAs are predicted to regulate the expression of ,50% of all protein coding genes in mammals. Therefore, they participate in virtually all cellular processes investigated so far. Altered miRNAs expressions are associated with both physiological (pregnancy) and pathological processes (cancer). As the dynamic maternal-fetal interface plays a critical role in the maintenance of successful pregnancy, it is not surprising that the miRNAs that are unique to reproductive tissues are abundantly expressed. Research in this field has demonstrated the presence and dysregulation of a distinct set of pregnancy-associated miRNAs; however, most studies have centered on localizing various miRNAs in reproductive microdomains associated with normal or complicated pregnancies. Although several independent miRNA regulatory mechanisms associated with endometrial receptivity, immune cells, angiogenesis and placental development have been studied, miRNA-mediated regulation of pregnancy remains poorly understood. This review provides a summary of the current data on miRNA regulation as well as functional profiles of miRNAs that are found in the uterus, in immune cells associated with maternal tolerance to the fetus, and those involved in angiogenesis and placental development.

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Section: Microrna Regulation In the Placentamentioning

confidence: 99%

Section: Microrna Regulation In the Placentamentioning

confidence: 99%

Section: Microrna Regulation In the Placentamentioning

confidence: 99%

Section: Microrna Regulation In the Placentamentioning

confidence: 99%

Section: Microrna Regulation In the Placentamentioning

confidence: 99%

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MicroRNAs, immune cells and pregnancy

et al. 2014

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miR‐346 and miR‐582‐3p‐regulated EG‐VEGF expression and trophoblast invasion via matrix metalloproteinases 2 and 9

Tsai

et al. 2016

BioFactors

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Endocrine gland-derived vascular endothelial growth factor (EG-VEGF) is an important regulator for embryo implantation and placental development, and is clinically associated with several obstetric disorders related to insufficient or inappropriate trophoblast invasion, such as recurrent abortion, preeclampsia, and intrauterine fetal growth restriction. This study was performed to identify the microRNAs targeting EG-VEGF, and evaluate the regulatory effect on trophoblast biology. miR-346 and miR-582-3p were initially identified via bioinformatic tools, and their specific binding sites on the EG-VEGF 3'UTR were further confirmed using dual luciferase and a co-transfection assays. miR-346 and miR-582-3p were demonstrated not only to suppress EG-VEGF expression, but also inhibit trophoblast invasion and migration in the JAR and HTR-8/SVneo cell lines. We further evaluated the effect of microRNAs in HTR-8/SVneo cells coexpressing EG-VEGF and miR-346 or miR-582-3p on matrix metalloproteinase (MMP 2 and MMP 9) and the tissue inhibitors of metalloproteinase (TIMP 1 and TIMP 2) using RT-PCR, western blotting and gelatin zymography. TIMP 1 and TIMP 2 were not affected by the two microRNAs, whereas the expressions and activities of MMP 2 and MMP 9 were significantly downregulated, which in turn inhibited the invasion ability of trophoblasts. In conclusion, miR-346 and miR-582-3p regulate EG-VEGF-induced trophoblast invasion through repressing MMP 2 and MMP 9, and may become novel diagnostic biomarkers or therapeutic targets for EG-VEGF-related obstetric disorders. © 2016 BioFactors, 43(2):210-219, 2017.

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Impact of Aging and Cellular Senescence in the Pathophysiology of Preeclampsia

Suvakov,

Kattah,

Gojkovic

et al. 2023

Comprehensive Physiology

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The incidence of hypertensive disorders of pregnancy is increasing, which may be due to several factors, including an increased age at pregnancy and more comorbid health conditions during reproductive years. Preeclampsia, the most severe hypertensive disorder of pregnancy, has been associated with an increased risk of future disease, including cardiovascular and kidney diseases. Cellular senescence, the process of cell cycle arrest in response to many physiologic and maladaptive stimuli, may play an important role in the pathogenesis of preeclampsia and provide a mechanistic link to future disease. In this article, we will discuss the pathophysiology of preeclampsia, the many mechanisms of cellular senescence, evidence for the involvement of senescence in the development of preeclampsia, as well as evidence that cellular senescence may link preeclampsia to the risk of future disease. Lastly, we will explore how a better understanding of the role of cellular senescence in preeclampsia may lead to therapeutic trials. © 2023 American Physiological Society. Compr Physiol 13:5077‐5114, 2023.

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Elevated levels of hypoxia‐inducible microRNA‐210 in pre‐eclampsia: new insights into molecular mechanisms for the disease

Cited by 206 publications

References 47 publications

MicroRNAs, immune cells and pregnancy

MicroRNAs, immune cells and pregnancy

miR‐346 and miR‐582‐3p‐regulated EG‐VEGF expression and trophoblast invasion via matrix metalloproteinases 2 and 9

Impact of Aging and Cellular Senescence in the Pathophysiology of Preeclampsia

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