PP088. The role of microRNA in pathogenesis of preeclampsia–miRNA network analysis

Lázár, Levente; Rigó, János

doi:10.1016/j.preghy.2013.04.113

Cited by 5 publications

(4 citation statements)

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“…miR-210 is upregulated by HIF which overexpresses it in response uteroplacental hypoxia in order to regulate genes involved in various pathways including angiogenesis, inflammation, and cell proliferation [ 87 ]. Another miRNA involved in preeclampsia is miR-155, which has been shown to inhibit cysteine-rich protein 61 (CYR61), an essential angiogenic factor in pregnancy [ 88 , 89 ]. A crucial function of CYR61 is related to inducing the expression of VEGF, which is a major pro-angiogenic factor as previously mentioned [ 87 ].…”

Section: Molecular Factors Resulting From Inadequate Uteroplacental Perfusion Leading To Preeclampsiamentioning

confidence: 99%

Defective Uteroplacental Vascular Remodeling in Preeclampsia: Key Molecular Factors Leading to Long Term Cardiovascular Disease

Hong

Kim

Hyun

et al. 2021

IJMS

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Preeclampsia is a complex hypertensive disorder in pregnancy which can be lethal and is responsible for more than 70,000 maternal deaths worldwide every year. Besides the higher risk of unfavorable obstetric outcomes in women with preeclampsia, another crucial aspect that needs to be considered is the association between preeclampsia and the postpartum cardiovascular health of the mother. Currently, preeclampsia is classified as one of the major risk factors of cardiovascular disease (CVD) in women, which doubles the risk of venous thromboembolic events, stroke, and ischemic heart disease. In order to comprehend the pathophysiology behind the linkage between preeclampsia and the development of postpartum CVD, a thorough understanding of the abnormal uteroplacental vascular remodeling in preeclampsia is essential. Therefore, this review aims to summarize the current knowledge of the defective process of spiral artery remodeling in preeclampsia and how the resulting placental damage leads to excessive angiogenic imbalance and systemic inflammation in long term CVD. Key molecular factors in the pathway—including novel findings of microRNAs—will be discussed with suggestions of future management strategies of preventing CVD in women with a history of preeclampsia.

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Section: Molecular Factors Resulting From Inadequate Uteroplacental Perfusion Leading To Preeclampsiamentioning

confidence: 99%

Defective Uteroplacental Vascular Remodeling in Preeclampsia: Key Molecular Factors Leading to Long Term Cardiovascular Disease

Hong

Kim

Hyun

et al. 2021

IJMS

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“…Another miRNA that is linked to PE is miR-155 ( 64 – 66 ). It is processed in humans from exon 3 of the non-protein coding B-cell integration cluster (BIC) RNA ( 67 ).…”

Section: The Role Of Mir-155 In Pementioning

confidence: 99%

MicroRNAs: New Players in the Pathobiology of Preeclampsia

Bounds

Chiasson

Pan

et al. 2017

Front. Cardiovasc. Med.

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Our understanding of how microRNAs (miRNAs) regulate gene networks and affect different molecular pathways leading to various human pathologies has significantly improved over the years. In contrary, the role of miRNAs in pregnancy-related hypertensive disorders such as preeclampsia (PE) is only beginning to emerge. Recent papers highlight that adverse pregnancy outcomes are associated with aberrant expression of several miRNAs. Presently, efforts are underway to determine the biologic function of these placental miRNAs which can shed light on their contribution to these pregnancy-related disease conditions. The discovery that miRNAs are stable in circulation coupled with the fact that the placenta is capable of releasing them to the circulation in exosomes generates a lot of enthusiasm to use them as biomarkers. In this review, we will summarize the recent findings of our understanding of miRNA regulation in relation to PE, a hypertensive disorder of pregnancy. Particular emphasis will be given to the role of key miRNA molecules such as miR-210 and miR-155 that are known to be consistently dysregulated in women with PE.

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“…The miRNA can intervene in various diseases by targeting and regulating gene expressions in a specific way. [5][6][7][8] It has been reported that the expression of miR-106a, a type of miRNA, can be downregulated in hypertension-induced heart failure, which affects the stress response in body and can be considered one of the influential factors in the treatment of hypertension-induced heart failure. [9][10][11][12] Mitogen-activated protein kinase (MAPK) pathway is believed to also participate in the regulation of stress response in body and be closely associated with GH.…”

Section: Introductionmentioning

confidence: 99%

“…MicroRNA (miRNA) is a small noncoding RNA molecule, existing in thousands of different kinds in tissues and cells. The miRNA can intervene in various diseases by targeting and regulating gene expressions in a specific way 5–8. It has been reported that the expression of miR‐106a, a type of miRNA, can be downregulated in hypertension‐induced heart failure, which affects the stress response in body and can be considered one of the influential factors in the treatment of hypertension‐induced heart failure 9–12.…”

Section: Introductionmentioning

confidence: 99%

Role of miR‐106‐mediated mitogen‐activated protein kinase signaling pathway in oxidative stress injury and inflammatory infiltration in the liver of the mouse with gestational hypertension

Wang

Bao

Song

et al. 2019

J of Cellular Biochemistry

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We aim to investigate the role of miR‐106‐mediated mitogen‐activated protein kinase (MAPK) signaling pathway in oxidative stress (OS) injury and inflammatory infiltration in the liver of the mouse with gestational hypertension (GH). Ninety specific pathogen‐free mice (Kunming species) during middle to late gestation were selected for the study. Fifteen mice were used as control, while the rest were used for establishing the GH model. The mice were assigned to six groups: normal group (normal gestation), model group (GH model), negative control group (GH model, intravenously injected with negative control vector), miR‐106a‐mimic group (GH model, intravenously injected with vector overexpressing miR‐106a, which mimics the overexpression of endogenous mature miR‐106a), SB203580 group (GH model, intravenously injected with MAPK pathway inhibitor SB203580), and miR‐106a‐mimic+SB203580 group (GH model, intravenously injected with SB203580 and vector overexpressing miR‐106a). Fourteen days after electrical stimulation, all the groups except for the normal group had elevated blood pressure vs those on day 0 and 7. Compared with the normal group, the other groups had lower levels of miR‐106a expression, nitric oxide, nitric oxide synthase, catalase, superoxide dismutase, S cell ratio, and interleukin‐4 (IL‐4) and IL‐10 in the serum and liver as opposed to increased levels of blood pressure, p38MAPK mRNA expression, p‐p38MAPK positive expression rate, protein expressions of p‐p38MAPK, p‐ERK, and p‐JNK, H2O2 and malondialdehyde in liver, G0/G1 cell ratio, apoptosis rate, and IL‐6, interferon‐γ (IFN‐γ), and IFN‐α in the serum and liver (all P < .05). The miR‐106 overexpression or inhibiting MAPK signaling pathway can attenuate OS injury and inflammatory response in the liver of the mouse with GH, and the effect can be even better if both miR‐106a overexpression and inhibiting MAPK pathway are applied. In conclusion, miR‐106a overexpression can inhibit OS injury and inflammatory infiltration in the liver of the mouse with GH by mediating MAPK signaling pathway.

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PP088. The role of microRNA in pathogenesis of preeclampsia–miRNA network analysis

Cited by 5 publications

References 0 publications

Defective Uteroplacental Vascular Remodeling in Preeclampsia: Key Molecular Factors Leading to Long Term Cardiovascular Disease

Defective Uteroplacental Vascular Remodeling in Preeclampsia: Key Molecular Factors Leading to Long Term Cardiovascular Disease

MicroRNAs: New Players in the Pathobiology of Preeclampsia

Role of miR‐106‐mediated mitogen‐activated protein kinase signaling pathway in oxidative stress injury and inflammatory infiltration in the liver of the mouse with gestational hypertension

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