MicroRNA-204 suppresses trophoblast-like cell invasion by targeting matrix metalloproteinase-9

Yu, Yang; Wang, Leilei; Liu, Tong; Guan, Hongyan

doi:10.1016/j.bbrc.2015.05.052

Cited by 57 publications

(52 citation statements)

References 27 publications

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“…MMP-2 and MMP-9 levels are also reduced in uterus, placenta and aorta of RUPP rats (Table 4), and low MMP levels may cause excessive collagen deposition, affect smooth muscle growth and decrease spiral arteries remodeling (Li et al, 2014b). Also, in an in vitro model of first trimester trophoblasts, suppression of MMP-9 expression inhibited TC invasive capability, supporting a role of MMP-9 in modulating trophoblast invasion (Yu et al, 2015). MMP-1 is also expressed in cytotrophoblasts and syncytiotrophoblasts of the placenta and decidua and may play a role in trophoblast invasion.…”

Section: Placental Ischemia As An Initiating Event In Preeclampsiamentioning

confidence: 72%

“…Genetic polymorphisms may alter MMP-2 and -9 transcription in PE (Palei et al, 2013a). Also, miRNA-519d-3p and miRNA-204 are overexpressed in PE patients (Choi et al, 2013; Li et al, 2013) and could target MMP-2 and MMP-9, respectively and in turn decrease trophoblast invasiveness (Yu et al, 2015) (Fig. 2).…”

Section: Placental Ischemia As An Initiating Event In Preeclampsiamentioning

confidence: 99%

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Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Possomato-Vieira

Khalil

2016

Advances in Pharmacology

185

117

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Preeclampsia is a pregnancy-related disorder characterized by hypertension, and could lead to maternal and fetal morbidity and mortality. Although the causative factors and pathophysiological mechanisms are unclear, endothelial dysfunction is a major hallmark of preeclampsia. Clinical tests and experimental research have suggested that generalized endotheliosis in the systemic, renal, cerebral and hepatic circulation could decrease endothelium-derived vasodilators such as nitric oxide, prostacyclin and hyperpolarization factor and increase vasoconstrictors such as endothelin-1 and thromboxane A2, leading to increased vasoconstriction, hypertension and other manifestation of preeclampsia. In search for the upstream mechanisms that could cause endothelial dysfunction, certain genetic, demographic and environmental risk factors have been suggested to cause abnormal expression of uteroplacental integrins, cytokines and matrix metalloproteinases, leading to decreased maternal tolerance, apoptosis of invasive trophoblast cells, inadequate spiral arteries remodeling, reduced uterine perfusion pressure (RUPP), and placental ischemia/hypoxia. RUPP may cause imbalance between the anti-angiogenic factors soluble fms-like tyrosine kinase-1 and soluble endoglin and the pro-angiogenic factors vascular endothelial growth factor and placental growth factor, or stimulate the release of other circulating bioactive factors such as inflammatory cytokines, hypoxia-inducible factor-1, reactive oxygen species, and angiotensin AT1 receptor agonistic autoantibodies. These circulating factors could then target endothelial cells and cause generalized endothelial dysfunction. Therapeutic options are currently limited, but understanding the factors involved in endothelial dysfunction could help design new approaches for prediction and management of preeclampsia.

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Section: Placental Ischemia As An Initiating Event In Preeclampsiamentioning

confidence: 72%

Section: Placental Ischemia As An Initiating Event In Preeclampsiamentioning

confidence: 99%

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Possomato-Vieira

Khalil

2016

Advances in Pharmacology

185

117

View full text Add to dashboard Cite

show abstract

“…Overall, expression levels of miR-486-5p increased by an average of 1.6-fold during pregnancy. Our other up-regulated miRNA, miR-204b, has an identical mature sequence to hsa-miR-204, which has been shown to be up-regulated in pre-eclampsia [26], potentially due to its role in suppressing trophoblast-like cell invasion [27]. …”

Section: Discussionmentioning

confidence: 99%

Evaluation of circulating miRNAs during late pregnancy in the mare

et al. 2017

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MicroRNAs (miRNAs) are small, non-coding RNAs which are produced throughout the body. Individual tissues tend to have a specific expression profile and excrete many of these miRNAs into circulation. These circulating miRNAs may be diagnostically valuable biomarkers for assessing the presence of disease while minimizing invasive testing. In women, numerous circulating miRNAs have been identified which change significantly during pregnancy-related complications (e.g. chorioamnionitis, eclampsia, recurrent pregnancy loss); however, no prior work has been done in this area in the horse. To identify pregnancy-specific miRNAs, we collected serial whole blood samples in pregnant mares at 8, 9, 10 m of gestation and post-partum, as well as from non-pregnant (diestrous) mares. In total, we evaluated a panel of 178 miRNAs using qPCR, eventually identifying five miRNAs of interest. One miRNA (miR-374b) was differentially regulated through late gestation and four miRNAs (miR-454, miR-133b, miR-486-5p and miR-204b) were differentially regulated between the pregnant and non-pregnant samples. We were able to identify putative targets for the differentially regulated miRNAs using two separate target prediction programs, miRDB and Ingenuity Pathway Analysis. The targets for the miRNAs differentially regulated during pregnancy were predicted to be involved in signaling pathways such as the STAT3 pathway and PI3/AKT signaling pathway, as well as more endocrine-based pathways, including the GnRH, prolactin and insulin signaling pathways. In summary, this study provides novel information about the changes occurring in circulating miRNAs during normal pregnancy, as well as attempting to predict the biological effects induced by these miRNAs.

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“…MicroRNA-155 inhibits migration of human HTR-8/ SVneo cell by downregulating cyclin D1 (Dai et al 2012). miRNA-204 suppresses the invasion of BeWo cells by reducing the expression of its target gene MMP9 (Yu et al 2015). miR-125b-1-3p inhibits trophoblast cell invasion by targeting S1PR1 in HTR8/SVneo cells (Li et al 2014a).…”

Section: R232mentioning

confidence: 99%

Progress in the understanding of the etiology and predictability of fetal growth restriction

Tang

Liu

et al. 2017

Reproduction

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Fetal growth restriction (FGR) is defined as the failure of fetus to reach its growth potential for various reasons, leading to multiple perinatal complications and adult diseases of fetal origins. Shallow extravillous trophoblast (EVT) invasion-induced placental insufficiency and placental dysfunction are considered the main reasons for idiopathic FGR. In this review, first we discuss the major characteristics of anti-angiogenic state and the pro-inflammatory bias in FGR. We then elaborate major abnormalities in placental insufficiency at molecular levels, including the interaction between decidual leukocytes and EVT, alteration of miRNA expression and imprinted gene expression pattern in FGR. Finally, we review current animal models used in FGR, an experimental intervention based on animal models and the progress of predictive biomarker studies in FGR. Free Chinese abstract: A Chinese translation of this abstract is freely available at http://www.reproduction-online.org/content/153/6/ R227/suppl/DC1. Reproduction (2017) 153 R227-R240

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MicroRNA-204 suppresses trophoblast-like cell invasion by targeting matrix metalloproteinase-9

Cited by 57 publications

References 27 publications

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Evaluation of circulating miRNAs during late pregnancy in the mare

Progress in the understanding of the etiology and predictability of fetal growth restriction

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