miR‐181a/b‐5p regulates human umbilical vein endothelial cell angiogenesis by targeting PDGFRA

Sun, Tingting; Yin, Linan; Kuang, Hongyu

doi:10.1002/cbf.3472

Cited by 18 publications

(9 citation statements)

References 19 publications

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“…The role of miR-181a-5p has been described in our previous study [ 15 ]. Overexpression of miR-181a-5p inhibits retinal neovascularization, which is consistent with other studies [ 27 , 28 ] and our RNA sequencing results. Jiang's report [ 29 ] revealed that miR-129-5p is highly expressed in prostate cancer tissues and overexpression of miR-129-5p significantly reduces cell migration, invasion, and angiogenesis.…”

Section: Discussionsupporting

confidence: 94%

“…Inversely, the expression levels of miR-181a-5P detected by qPCR were significantly lower in the OIR group than in the NOR group, in accordance with our RNA sequencing results. Sun [ 27 ] reported that overexpression of miR-181a/b-5p reduced cellular proliferation, migration, invasion, and tube formation. Li [ 28 ] reported that miR-181a-5p decreased the migration and invasion of cancer cell by targeting the matrix metalloproteinase-14.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA Expression Analysis of Mice Retinas with Oxygen-Induced Retinopathy by RNA Sequencing

Chen

Liu

et al. 2022

Journal of Ophthalmology

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Purpose. To characterize the microRNA (miRNA) expression profiles in the retinas of mice with oxygen-induced retinopathy by RNA sequencing and to ascertain miRNAs associated with retinal neovascularization. Methods. Retina samples were obtained from 3 groups (6 retinas/group) of OIR mice and normal mice at P17. RNA was isolated from 24 retina samples and then detected on an Illumina HiSeq. Twelve retina samples were used for quantitative polymerase chain reaction to validate the RNA sequencing. Bioinformatics analyses were performed. Result. The RNA sequence showed that 565 miRNAs were detected in the retina of OIR mice and 583 miRNAs in the retina of normal control mice. A total of 553 miRNAs were expressed in both groups. Thirty-eight miRNAs showed altered expression in both groups ( p ≤ 0.05 ). Compared with the control group, 2 miRNAs were significantly upregulated in the OIR group, while 36 miRNAs were significantly downregulated. Meanwhile, 2 candidate miRNAs (miR-181a-5p and miR-21a-5p) with significant differences in miRNA expression ( p < 0.01 ) were selected for validation. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to confirm the relative expression of the two miRNAs. Bioinformatics analyses showed that pathways involved in ischemic retinopathy (such as TGF-β, Ras, Hippo, PI3K-Akt, VEGF, and HIF-1 signaling pathways) were enriched. Conclusions. Our study provided an overall view of miRNA profiling in the OIR retina. These miRNA profiles provide a valuable framework for the potential therapy of retinal angiogenesis.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

MicroRNA Expression Analysis of Mice Retinas with Oxygen-Induced Retinopathy by RNA Sequencing

Chen

Liu

et al. 2022

Journal of Ophthalmology

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“…Based on pathway analysis of miRNA target genes, this subset of miRNAs acts in concert to induce cell cycle phase arrest and telomere erosion, establishing a senescent phenotype. In addition, miR-181a/b and miR-221 have been reported to modulate angiogenesis by targeting platelet-derived growth factor receptor A (PDGFRA) [52], and tissue inhibitor of metalloproteinase 3 (TIMP3) and hypoxia-inducible factor 1-α (HIF1A) [53,54], respectively. miR-222-3p inhibits migration and tube formation in endothelial progenitor cells by targeting adiponectin receptor 1 (ADIPOR1) [55].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-Mediated Downregulation of HMGB2 Contributes to Cellular Senescence in Microvascular Endothelial Cells

Jeong

2022

Cells

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High mobility group box 2 (HMGB2) is a non-histone chromosomal protein involved in various biological processes, including cellular senescence. However, its role in cellular senescence has not been evaluated extensively. To determine the regulatory role and mechanism of HMGB2 in cellular senescence, we performed gene expression analysis, senescence staining, and tube formation assays using young and senescent microvascular endothelial cells (MVECs) after small RNA treatment or HMGB2 overexpression. HMGB2 expression decreased with age and was regulated at the transcriptional level. siRNA-mediated downregulation inhibited cell proliferation and accelerated cellular senescence. In contrast, ectopic overexpression delayed senescence and maintained relatively higher tube-forming activity. To determine the HMGB2 downregulation mechanism, we screened miRNAs that were significantly upregulated in senescent MVECs and selected HMGB2-targeting miRNAs. Six miRNAs, miR-23a-3p, 23b-3p, -181a-5p, -181b-5p, -221-3p, and -222-3p, were overexpressed in senescent MVECs. Ectopic introduction of miR-23a-3p, -23b-3p, -181a-5p, -181b-5p, and -221-3p, with the exception of miR-222-3p, led to the downregulation of HMGB2, upregulation of senescence-associated markers, and decreased tube formation activity. Inhibition of miR-23a-3p, -181a-5p, -181b-5p, and -221-3p delayed cellular senescence. Restoration of HMGB2 expression using miRNA inhibitors represents a potential strategy to overcome the detrimental effects of cellular senescence in endothelial cells.

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“…6B-E) results demonstrated that knockdown of SOCS1 reduced SOCS1 expression in HTR8+ siSOCS1 group compared with that in the HTR + NC group, but IFN-γ intervention increased SOCS1 expression in HTR8 + IFN-γ + siSOCS1 group compared with that in the HTR + siSOCS1 group. Compared with the siNC group, western blot analysis indicated that EZR and PDGFRA expressions, which is related to cell invasion and migration respectively (19,20), were reduced in the siSOCS1 group; whilst the expression of cell apoptosis marker cleaved caspase3 was increased in the siSOCS1 group ( Fig. 6B and C).…”

Section: Socs1 Silencing F Urther Inhibits Ifn-γ-mediatedmentioning

confidence: 92%

Increased expression of IFN‑γ in preeclampsia impairs human trophoblast invasion via a SOCS1/JAK/STAT1 feedback loop

2020

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The weakening of extravillous trophoblast (EVT) invasion results in shallow placenta implantation. In HTR8/SVneo cells, IFN-γ can activate STAT1 and reduce cell invasion, and suppressor of cytokine signaling (SOCS) is an important negative regulatory protein in the Janus kinase (JAK)/STAT activator pathway and has a negative feedback function on JAK/STAT1. The aim of the present study was to elucidate how SOCS1 feedback regulates JAK/STAT1 and affects EVT cell invasion, which in turn affects the development of preeclampsia (PE). MTT and Annexin V/phosphatidylserine (PS) assays were performed to evaluate the viability and apoptosis of HTR8/SVneo cells treated with IFN-γ, respectively. Wound healing and invasion assays were also conducted to measure the migratory and invasive abilities of IFN-γ-treated HTR8/SVneo cells. The mRNA and protein expression levels of genes were detected using reverse transcription-quantitative PCR and western blot analysis. Small interfering RNA knockdown of SOCS1 was used to verify the role of feedback regulation in the IFN-γ-activated JAK/STAT1 signaling pathway. IFN-γ can inhibit HTR8/SVneo migration and invasion, and promote apoptosis by increasing the expression of phosphorylated (p)-JAK, p-STAT1 and caspase3, and reducing the expression of platelet-derived growth factor receptor A and Ezrin. Furthermore, SOCS1 may negatively regulate JAK/STAT1 and affect HTR-8/SVneo invasiveness. Evaluation of clinical samples demonstrated that the expression levels of SOCS1 and IFN-γ were higher in patients with PE compared with the healthy group. Collectively, the present results indicated that IFN-γ reduced the invasion of HTR-8/SVneo cells by activating JAK/STAT1, concurrently leading to an increase in SOCS1, which negatively regulates JAK/STAT1 and eliminates the pro-inflammatory effects of IFN-γ, thus forming a feedback loop.

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miR‐181a/b‐5p regulates human umbilical vein endothelial cell angiogenesis by targeting PDGFRA

Cited by 18 publications

References 19 publications

MicroRNA Expression Analysis of Mice Retinas with Oxygen-Induced Retinopathy by RNA Sequencing

MicroRNA Expression Analysis of Mice Retinas with Oxygen-Induced Retinopathy by RNA Sequencing

MicroRNA-Mediated Downregulation of HMGB2 Contributes to Cellular Senescence in Microvascular Endothelial Cells

Increased expression of IFN‑γ in preeclampsia impairs human trophoblast invasion via a SOCS1/JAK/STAT1 feedback loop

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