MicroRNAs: Potential Targets in Diabetic Retinopathy

Li, Xin; Yu, Zi-Wei; Wang, Ying; Fu, Yuhong; Gao, Xinyuan

doi:10.1055/a-1107-2943

Cited by 24 publications

(22 citation statements)

References 87 publications

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“…Furthermore, differentially expressed miRNAs function as diagnostic biomarkers for diabetic retinopathy [ 29 , 50 ]. Numerous studies have investigated the role of miR-192 in various diabetic complications [ 51 , 52 ]. In diabetic nephropathy, the expression levels of miR-192 are closely associated with disease progression, suggesting its potential as an indicator in the diagnosis and determination of diabetic nephropathy [ 53–56 ].…”

Section: Discussionmentioning

confidence: 99%

MiR-192 attenuates high glucose-induced pyroptosis in retinal pigment epithelial cells via inflammasome modulation

Zhang

et al. 2022

Bioengineered

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Diabetic retinopathy is one of the most characteristic complications of diabetes mellitus, and pyroptosis plays acrucial role in the onset and development of diabetic retinopathy. Although microRNA-192 (miR-192) has been demonstrated to be involved in diabetic retinopathy progression, to the best of our knowledge, its potential and mechanism in cell pyroptosis in diabetic retinopathy have not been studied. The present study demonstrated that high glucose (HG) contributes to the pyroptosis of retinal pigment epithelial (RPE) cells in a dose-dependent manner. The results revealed that miR-192 was weakly expressed in HG-induced RPE cells. Furthermore, overexpression of miR-192 abrogated the role of HG in RPE cell pyroptosis. Based on the bioinformatics analysis, a dual-luciferase reporter assay, and an RNA pull-down assay, FTO α-ketoglutarate-dependent dioxygenase (FTO) was demonstrated to be a direct target of miR-192. Additionally, upregulation of FTO abolished the effects of miR-192 on RPE cells treated with HG. Nucleotide-binding domain leucine-rich repeat family protein 3 (NLRP3) inflammasome activation is vital for cell pyroptosis, and FTO functions as a pivotal modulator in the N 6 -methyladenosine modifications of various genes. Mechanistically, FTO enhanced NLRP3 expression by facilitating demethylation of NLRP3. In conclusion, the present results demonstrate that miR-192 represses RPE cell pyroptosis triggered by HG via regulation of the FTO/NLRP3 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

MiR-192 attenuates high glucose-induced pyroptosis in retinal pigment epithelial cells via inflammasome modulation

Zhang

et al. 2022

Bioengineered

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“…29 Increased DKK1 expression inhibits the activity of Wnt/β-catenin signaling pathway, which in turn restrains trophoblast cell migration and invasion. 30 Wnt/β-catenin signaling pathway may play a significant role in the pathogenesis of PE. Given related previous conclusions, it could be speculated that the Wnt/β-catenin pathway manages cell function in trophoblasts.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of ALKBH5‐mediated m⁶A modification of PPARG mRNA alleviates H/R‐induced oxidative stress and apoptosis in placenta trophoblast

Guo

Song

Yang

2022

Environmental Toxicology

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The alpha-ketoglutarate-dependent (ALKB) homolog 5 (ALKBH5), an m 6 A demethylase, has been reported to be involved in the pathogenesis of preeclampsia (PE), but the exact mechanism requires further investigation. RT-qPCR or Western blotting were used to determine ALKBH5 and peroxisome proliferator-activated receptor gamma (PPARG) expression in placentas from PE patients and normal volunteers, as well as in HTR-8/SVneo cells treated with hypoxia/reoxygenation (H/R).Our results showed that the expression of ALKBH5 was significantly upregulated and PPARG was downregulated in preeclamptic placentas and H/R-treated cells.ALKBH5 interference reduced m 6 A levels of PPARG mRNA, and increased PPARG mRNA stability and promoted PPARG translation level. In addition, ALKBH5 silencing increased the cell proliferation, migration, and vimentin protein level, and inhibited cell apoptosis, oxidative stress, and protein levels of endoglin (ENG) and E-cadherin in H/R-treated cells, whereas PPARG interference reversed these effects. Furthermore, PPARG repressed the H3K9me2 levels at activated leukocyte cell adhesion molecule (ALCAM) promoter region by increasing the expression and activity of lysine demethylase 3B (KDM3B). ALCAM inhibition reversed the effects of PPARG overexpression on H/R-treated cell functions. PKF115-584 suppressed the effects of

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“…Lately, miRNA-non-coding, short (around 22 nucleotides), single-stranded RNA molecules have also been highlighted as potential therapeutic tools and diagnostic markers [17][18][19][20]. miRNAs are able to interact with mRNA strains, inhibiting them, thus reducing protein expression.…”

Section: Introductionmentioning

confidence: 99%

Oxidative-Induced Angiogenesis Is Modulated by Small Extracellular Vesicle miR-302a-3p Cargo in Retinal Pigment Epithelium Cells

et al. 2022

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Extracellular vesicles are released from cells under diverse conditions. Widely studied in cancer, they are associated with different diseases playing major roles. Recent reports indicate that oxidative damage promotes the release of small extracellular vesicle (sEVs) from the retinal pigment epithelium (RPE), with an angiogenic outcome and changes in micro-RNA (miRNA) levels. The aim of this study was to determine the role of the miRNA miR-302a-3p, included within RPE-released sEVs, as an angiogenic regulator in cultures of endothelial cells (HUVEC). ARPE-19 cell cultures, treated with H2O2 to cause an oxidative insult, were transfected with a miR-302a-3p mimic. Later, sEVs from the medium were isolated and added into HUVEC or ARPE-19 cultures. sEVs from ARPE-19 cells under oxidative damage presented a decrease of miR-302a-3p levels and exhibited proangiogenic properties. In contrast, sEVs from miR-302a-3p-mimic transfected cells resulted in control angiogenic levels. The results herein indicate that miR-302a-3p contained in sEVs can modify VEGFA mRNA expression levels as part of its antiangiogenic features.

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MicroRNAs: Potential Targets in Diabetic Retinopathy

Cited by 24 publications

References 87 publications

MiR-192 attenuates high glucose-induced pyroptosis in retinal pigment epithelial cells via inflammasome modulation

MiR-192 attenuates high glucose-induced pyroptosis in retinal pigment epithelial cells via inflammasome modulation

Inhibition of ALKBH5‐mediated m⁶A modification of PPARG mRNA alleviates H/R‐induced oxidative stress and apoptosis in placenta trophoblast

Oxidative-Induced Angiogenesis Is Modulated by Small Extracellular Vesicle miR-302a-3p Cargo in Retinal Pigment Epithelium Cells

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MicroRNAs: Potential Targets in Diabetic Retinopathy

Cited by 24 publications

References 87 publications

MiR-192 attenuates high glucose-induced pyroptosis in retinal pigment epithelial cells via inflammasome modulation

MiR-192 attenuates high glucose-induced pyroptosis in retinal pigment epithelial cells via inflammasome modulation

Inhibition of ALKBH5‐mediated m6A modification of PPARG mRNA alleviates H/R‐induced oxidative stress and apoptosis in placenta trophoblast

Oxidative-Induced Angiogenesis Is Modulated by Small Extracellular Vesicle miR-302a-3p Cargo in Retinal Pigment Epithelium Cells

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Inhibition of ALKBH5‐mediated m⁶A modification of PPARG mRNA alleviates H/R‐induced oxidative stress and apoptosis in placenta trophoblast