micro<scp>RNA</scp>‐181a inhibits ocular neovascularization by interfering with vascular endothelial growth factor expression

Yang, Chun; Tahiri, Houda; Cai, ChenRongRong; Gu, Muqing; Gagnon, Carmen; Hardy, Pierre

doi:10.1111/1755-5922.12329

Cited by 19 publications

(11 citation statements)

References 59 publications

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“…miR‐181a is known to exert a strong antiangiogenic effect on RNV (Yang et al, 2018); however, miR‐181a‐5p target genes and its role in RNV have not yet been fully elucidated. Accumulating evidence suggests that the ERK pathway plays a crucial role in various cellular events, including angiogenesis (Koch, Tugues, Li, Gualandi, & Claesson‐Welsh, 2011; Lemmens, Kusters, Bronckaers, Geurts, & Hendrix, 2017), while endocan deficiency has been shown to decrease p‐ERK1/2 levels (Rocha et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of miR‐181a‐5p inhibits retinal neovascularization through endocan and the ERK1/2 signaling pathway

Chen

Yao

Yuan

et al. 2020

Journal Cellular Physiology

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Retinal neovascularization (RNV) is a common pathological feature of angiogenesis‐related retinopathy. Endocan inhibition has previously been reported to suppress RNV in oxygen‐induced retinopathy (OIR); however, its molecular mechanisms remain to be elucidated. Here, we investigated the role and mechanism of endocan in OIR. We established an OIR mouse model and detected aberrant endocan overexpression in OIR mouse retinas. Endocan inhibition through small interfering RNA or a neutralizing antibody inhibited vascular endothelial growth factor‐induced cell survival, cell proliferation, and tube formation in human retinal endothelial cells in vitro and reduced the RNV area in vivo. Using RNA sequencing, a luciferase reporter assay, and bioinformatics analyses, we identified endocan as a microRNA‐181a‐5p target gene. The antiangiogenic effect of miR‐181a‐5p on RNV was verified by intravitreal injection, and we showed that this involved the extracellular signal‐regulated protein kinases 1 and 2 (ERK1/2) signaling pathway. Collectively, our data demonstrate that miR‐181a‐5p/endocan regulates retinal angiogenesis through the ERK1/2 signaling pathway and might represent an attractive therapeutic strategy for RNV.

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Section: Discussionmentioning

confidence: 99%

Overexpression of miR‐181a‐5p inhibits retinal neovascularization through endocan and the ERK1/2 signaling pathway

Chen

Yao

Yuan

et al. 2020

Journal Cellular Physiology

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“…Further, overexpression of these mitomiRs was found to decrease Bcl-2 expression, leading to mitochondrial permeability transition pore opening, activation of caspase-1 and 3, and cell apoptosis [98]. MitomiRs has been demonstrated to inhibit angiogenesis and vascularization [102]; however, the molecular mechanisms involved in mitomiRs-inhibited angiogenesis, with particular emphasis on those associated with cardiovascular disease, need further investigation.…”

Section: Mirnas That Inhibit Angiogenesismentioning

confidence: 99%

Mitochondrial MiRNA in Cardiovascular Function and Disease

Song

Zhang

2019

Cells

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MicroRNAs (miRNAs) are small noncoding RNAs functioning as crucial post-transcriptional regulators of gene expression involved in cardiovascular development and health. Recently, mitochondrial miRNAs (mitomiRs) have been shown to modulate the translational activity of the mitochondrial genome and regulating mitochondrial protein expression and function. Although mitochondria have been verified to be essential for the development and as a therapeutic target for cardiovascular diseases, we are just beginning to understand the roles of mitomiRs in the regulation of crucial biological processes, including energy metabolism, oxidative stress, inflammation, and apoptosis. In this review, we summarize recent findings regarding how mitomiRs impact on mitochondrial gene expression and mitochondrial function, which may help us better understand the contribution of mitomiRs to both the regulation of cardiovascular function under physiological conditions and the pathogenesis of cardiovascular diseases.

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“…miRNAs exert multiple types of functions including regulation of inflammatory, oxidative stress, angiogenesis, and coagulation in the progression and development of DR. [21][22][23] For instance, the ectopic expressions of miR-21-5p, miR-365, miR-495, or miR-211 promoted cell proliferation and angiogenesis in DR by modulation of maspin/ AKT/ERK, Timp3, Notch/PTEN/Akt, or Sirtuin 1, respectively, [24][25][26][27] while miR-384-3p, miR-145, miR-133b, or miR-181a suppressed retinal neovascularization, oxidative stress, inflammation, and cell proliferation via restraining hexokinase 2, TLR4/NF-κB, ras homolog family member A, or VEGF expressions, respectively. [28][29][30] Although miR-142 has been considered as one of leading functional miRNAs in various cellular events, studies reported that miR-142-5p was implicated in occurrence and progression of DM and its complications. 9,12 In DM human subjects as well as in mouse models, miR-142 level was reduced.…”

Section: Discussionmentioning

confidence: 99%

miR-142-5p regulates the progression of diabetic retinopathy by targeting IGF1

Liu

2020

Int J Immunopathol Pharmacol

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As one of leading causes of blindness, diabetic retinopathy (DR) is a progressive microvascular complication of diabetes mellitus (DM). Despite significant efforts have been devoted to investigate DR over the years, the molecular mechanisms still remained unclear. Emerging evidences demonstrated that microRNAs (miRNAs) were tightly associated with pathophysiological development of DR. Hence, this study was aimed to illustrate the role and molecular mechanisms of miR-412-5p in progression of DR. Streptozotocin (STZ) treatment in rats and human retinal endothelial cell (HREC) models were used to simulate DR conditions in vivo and in vitro. Hematoxylin-eosin (HE) staining was used to demonstrate the morphology of retinal tissues of rats. Qualitative real-time polymerase chain reaction (qRT-PCR) detected miR-142-5p and vascular endothelial growth factor (VEGF) expression levels. Cell counting kit-8 (CCK8) assay and immunofluorescence (IF) measured the cell proliferation rates. Western blot tested the expression status of IGF1/IGF1R-mediated signaling pathway. Dual-luciferase reporter assays demonstrated the molecular mechanism of miR-142-5p. miR-142-5p level was down-regulated in retinal tissues of DR rats and high glucose (HG)-treated HRECs. Insulin-like growth factor 1 (IGF1) was identified as a direct target of miR-142-5p. The reduced miR-142-5p level enhanced HRECs proliferation via activating IGF/IGF1R-mediated signaling pathway including p-PI3K, p-ERK, p-AKT, and VEGF activation, ultimately giving rise to cell proliferation. Either miR-142-5p overexpression or IGF1 knockdown alleviated the pathological effects on retinal tissues in DR rats. Collectively, miR-142-5p participated in DR development by targeting IGF1/p-IGF1R signaling pathway and VEGF generation. This miR-142-5p/IGF1/VEGF axis provided a novel therapeutic target for DR clinical treatment.

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microRNA‐181a inhibits ocular neovascularization by interfering with vascular endothelial growth factor expression

Abstract: These data may open unexpected avenues for the development of miR-181a as a novel therapeutic strategy that would be particularly useful and relevant for the treatment of neovascular diseases.

Cited by 19 publications

References 59 publications

Overexpression of miR‐181a‐5p inhibits retinal neovascularization through endocan and the ERK1/2 signaling pathway

Overexpression of miR‐181a‐5p inhibits retinal neovascularization through endocan and the ERK1/2 signaling pathway

Mitochondrial MiRNA in Cardiovascular Function and Disease

miR-142-5p regulates the progression of diabetic retinopathy by targeting IGF1

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