Early-onset preeclampsia, plasma microRNAs, and endothelial cell function

Lip, Simone V.; Boekschoten, Mark V.; Hooiveld, Guido; Pampus, Maria G. van; Scherjon, Sicco A.; Plösch, Torsten; Faas, Marijke M.

doi:10.1016/j.ajog.2019.11.1286

Cited by 35 publications

(22 citation statements)

References 51 publications

(50 reference statements)

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“…mir-574-5p, mir-1972, and mir-4793 have been identified as elevated in preeclampsia relative to healthy patients with the greatest fold change and lowest false discovery rate. 65 All three have been linked to endothelial dysfunction including impaired wound healing and decreasing proliferation.…”

Section: Endothelial Rnasmentioning

confidence: 99%

Clinical tools and biomarkers to predict preeclampsia

et al. 2022

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Preeclampsia is pregnancy-specific, and significantly contributes to maternal, and perinatal morbidity and mortality worldwide. An effective predictive test for preeclampsia would facilitate early diagnosis, targeted surveillance and timely delivery; however limited options currently exist. A first-trimester screening algorithm has been developed and validated to predict preterm preeclampsia, with poor utility for term disease, where the greatest burden lies. Biomarkers such as sFlt-1 and placental growth factor are also now being used clinically in cases of suspected preterm preeclampsia; their high negative predictive value enables confident exclusion of disease in women with normal results, but sensitivity is modest. There has been a concerted effort to identify potential novel biomarkers that might improve prediction. These largely originate from organs involved in preeclampsia's pathogenesis, including placental, cardiovascular and urinary biomarkers. This review outlines the clinical imperative for an effective test and those already in use and summarises current preeclampsia biomarker research.

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Section: Endothelial Rnasmentioning

confidence: 99%

Clinical tools and biomarkers to predict preeclampsia

et al. 2022

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“…or migration as well as tube formation of ECs in preeclampsia (33). However, whether miR-1972 exert the similar role in RA is unknown.…”

Section: Graphical Abstract |mentioning

confidence: 99%

RA Fibroblast-Like Synoviocytes Derived Extracellular Vesicles Promote Angiogenesis by miRNA-1972 Targeting p53/mTOR Signaling in Vascular Endotheliocyte

et al. 2022

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Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammatory in joints. Invasive pannus is a characteristic pathological feature of RA. RA fibroblast-like synoviocytes (FLSs) are showed tumor-like biological characters that facilitate pannus generation. Importantly, it has been documented that extracellular vesicle (EVs) derived microRNAs have a vital role of angiogenesis in various immune inflammatory diseases. However, whether RA FLSs derived EVs can facilitate angiogenesis and the underlying mechanism is undefined. Herein, we aim to investigate the key role of RA FLSs derived EVs on angiogenesis in endothelial cells (ECs). We indicate that RA FLSs derived EVs promote ECs angiogenesis by enhancing migration and tube formation of ECs in vitro. Also, we confirm that RA FLSs derived EVs can significantly facilitate ECs angiogenesis with a matrigel angiogenesis mice model. In terms of the mechanisms, both RNAs and proteins in EVs play roles in promoting ECs angiogenesis, but the RNA parts are more fundamental in this process. By combining microRNA sequencing and qPCR results, miR-1972 is identified to facilitate ECs angiogenesis. The blockage of miR-1972 significantly abrogated the angiogenesis stimulative ability of RA FLSs derived EVs in ECs, while the overexpression of miR-1972 reversed the effect in ECs. Specifically, the p53 level is decreased, and the phosphorylated mTOR is upregulated in miR-1972 overexpressed ECs, indicating that miR-1972 expedites angiogenesis through p53/mTOR pathway. Collectively, RA FLSs derived EVs can promote ECs angiogenesis via miR-1972 targeted p53/mTOR signaling, targeting on RA FLSs derived EVs or miR-1972 provides a promising strategy for the treatment of patients with RA.

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“…Images of three random visual fields of each group were captured using a bright-field microscope (magnification, x40) at 0 and 24 h after scratching. The width of the healed wound was quantified using ImageJ software (v1.52a; National Institutes of Health), and the migratory rate was calculated (32,33).…”

Section: -Ethynyl-2'-deoxyuridine (Edu) Assaymentioning

confidence: 99%

A novel peptide relieves endothelial cell dysfunction in preeclampsia by regulating the PI3K/mTOR/HIF1α pathway

Xue

Xie

et al. 2020

Int J Mol Med

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Preeclampsia (PE) is a pregnancy-specific complication characterized by hypertension and proteinuria, and it is one of the primary global causes of maternal and perinatal mortality. Poor remodeling of placental arteries and endothelial dysfunction serve important roles in the pathogenesis of PE. Peptide derived from complement C4 A chain (PDCC4) was identified in our previous peptidome analysis of serum from patients with PE. The present study aimed to investigate the effect of PDCC4 on endothelial dysfunction in PE. TNF-α stimulated HUVECs were employed to mimic endothelial dysfunction in PE, and Cell Counting Kit 8 assay, wound healing assay, tube formation assay, RNA-sequencing (seq) and western blot analysis were performed using HUVECs. Moreover, an in vivo model of PE was established using pregnant rats treated with lipopolysaccharide (LPS), and blood pressure monitoring, histopathological examination, ELISA and immunohistochemistry were performed on rats. It was found that TNF-α impaired proliferation, migration and tube formation of HUVECs, but pretreatment with PDCC4 moderated these effects. RNA-seq and western blotting demonstrated that the PI3K/mTOR/HIF1α signaling pathway was activated by PDCC4, and a selective PI3K inhibitor reversed the protective function of PDCC4 on TNF-α stimulated HUVECs. Additionally, PDCC4 alleviated hypertension, histopathological changes of placenta and kidney and the expression levels of endothelial injury markers and inflammatory cytokines induced by LPS in rats. These results suggested that PDCC4 relieved endothelial dysfunction in PE via PI3K/mTOR/HIF1α signaling pathway and may be a potential therapy for PE.

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Early-onset preeclampsia, plasma microRNAs, and endothelial cell function

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Cited by 35 publications

References 51 publications

Clinical tools and biomarkers to predict preeclampsia

Clinical tools and biomarkers to predict preeclampsia

RA Fibroblast-Like Synoviocytes Derived Extracellular Vesicles Promote Angiogenesis by miRNA-1972 Targeting p53/mTOR Signaling in Vascular Endotheliocyte

A novel peptide relieves endothelial cell dysfunction in preeclampsia by regulating the PI3K/mTOR/HIF1α pathway

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