MiR-30a inhibits BECN1-mediated autophagy in diabetic cataract

Zhang, Lu; Cheng, Rong; Huang, Yusen

doi:10.18632/oncotarget.20483

Cited by 35 publications

(29 citation statements)

References 44 publications

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“…Globally, age‐related cataract is one of the prior causes of blindness and the incidence rates of cataract are even rising, primarily owing to an increase in relative risk factors encompassing smoking, alcohol consumption, hyperglycemia, and hypertension . There have numerous studies concerned with the underlying mechanism aiming to explore novel targets for age‐related cataract therapy. Thus, the amenable molecular targeted treatment of this disease is still in demand.…”

Section: Introductionmentioning

confidence: 99%

miR‐23b‐3p regulates apoptosis and autophagy via suppressing SIRT1 in lens epithelial cells

Zhou

Wang

et al. 2019

J of Cellular Biochemistry

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Age-related cataract is one of the prior causes of blindness and the incidence rates of cataract are even rising. Oxidative stress plays an important role in the pathogenesis of cataracts. Under oxidative stress, lens epithelial cell (LEC cell) apoptosis is activated, which might lead to the opacity of the lens and accelerate the progression of cataract development. Meanwhile, autophagy is also active to face oxidative stress. miRNAs have been reported to involve cataract. However, the underlying mechanism is not clear. The present study aimed to investigate the regulatory effect of miR23b-3p on apoptosis and autophagy in LEC cells under oxidative stress. The expression levels of miR-23b-3p were examined in age-related cataract tissues and LEC cells treated with hydrogen peroxide, showing that miR23b-3p expression levels were upregulated. Knockdown of miR23b-3p expression in LEC cells brought about apoptosis significantly decreased while autophagy significantly increased during hydrogen peroxide.We predicted microRNA miRNA-23b-3p might participate in regulating silent information regulator 1 (SIRT1) by bioinformatics database of TargetScan. Luciferase reporter assays confirmed that miRNA-23b-p could suppress SIRT1 expression by binding its 3′UTR. In addition, overexpression or knockdown of miR-23b-3p could decrease or increase SIRT1 expression, which indicated that Mir-23b-3p could suppress SIRT1 expression. In addition, enhanced SIRT1 could attenuate the regulation of cell apoptosis and autophagy induced by overexpression of miR-23b-3p. Taken together, our findings revealed that miR-23b-3p regulated apoptosis and autophagy via suppressing SIRT1 in LEC cell under oxidative stress, which could provide new ideas for clinical treatment of cataract. K E Y W O R D Sapoptosis, autophagy, cataract, miR-23b-p, SIRT1

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Section: Introductionmentioning

confidence: 99%

miR‐23b‐3p regulates apoptosis and autophagy via suppressing SIRT1 in lens epithelial cells

Zhou

Wang

et al. 2019

J of Cellular Biochemistry

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“…In addition to lens development, differential regulation of miR-204 has been associated with loss of lens transparency or cataract formation in humans and mice, including agerelated cataract, congenital cataract, diabetic cataract, and secondary (post-surgical) cataract or posterior capsular opacification (PCO)-a post-operative complication of cataract surgery [172][173][174][175][176][177]. Microarray analysis has revealed downregulation (> 2-fold) of miR-204-5p and miR-204-3p in central, anterior lens epithelium (capsulorrhexis) samples from patients undergoing age-related cataract surgery [173,175] and miR-204-5p was one of the five most downregulated (~60-fold) microRNAs in diabetic cataract [177]. Significant downregulation of miR-204-5p (~67-fold) and miR-204-3p (> 12-fold) has also been associated with the human donor lens 'capsular-bag' model of PCO in vitro [176].…”

Section: Mir-204 In Cataractmentioning

confidence: 99%

TRPM3_miR-204: a complex locus for eye development and disease

Shiels

2020

Hum Genomics

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First discovered in a light-sensitive retinal mutant of Drosophila, the transient receptor potential (TRP) superfamily of non-selective cation channels serve as polymodal cellular sensors that participate in diverse physiological processes across the animal kingdom including the perception of light, temperature, pressure, and pain. TRPM3 belongs to the melastatin sub-family of TRP channels and has been shown to function as a spontaneous calcium channel, with permeability to other cations influenced by alternative splicing and/or non-canonical channel activity. Activators of TRPM3 channels include the neurosteroid pregnenolone sulfate, calmodulin, phosphoinositides, and heat, whereas inhibitors include certain drugs, plant-derived metabolites, and G-protein subunits. Activation of TRPM3 channels at the cell membrane elicits a signal transduction cascade of mitogen-activated kinases and stimulus response transcription factors. The mammalian TRPM3 gene hosts a non-coding microRNA gene specifying miR-204 that serves as both a tumor suppressor and a negative regulator of post-transcriptional gene expression during eye development in vertebrates. Ocular co-expression of TRPM3 and miR-204 is upregulated by the paired box 6 transcription factor (PAX6) and mutations in all three corresponding genes underlie inherited forms of eye disease in humans including early-onset cataract, retinal dystrophy, and coloboma. This review outlines the genomic and functional complexity of the TRPM3_miR-204 locus in mammalian eye development and disease.

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“…In ARC, miRNA-34a was upregulated and acted on Notch2, Bcl-2 and SIRT1 and causes apoptosis of HLECs [20] [25]. In DC, miRNA-30a was downregulated and regulated the EMT and autophagy by different pathways [22] [23].…”

Section: The Expression and Function Of Mirna In The Cataractmentioning

confidence: 99%

The Emerging Roles of Non-Coding RNAs in Cataract

Li¹,

Lei²,

Wang³

et al. 2020

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Non-coding RNAs (ncRNAs) are a large class of transcripts lacking evident protein coding potential, and play versatile roles in a diverse range of physiological and pathological processes. Mounting evidences have indicated that ncRNAs are aberrantly expressed in a wealth of diseases such as cataract. Cataract is a cloudy lens caused by radiation, age, drugs and other factors. NcRNAs, including microRNAs, long non-coding RNAs, circular RNAs, have been identified to regulate the occurrence and development of cataract. Current studies indicate that ncRNAs exert the multifaceted functions in the lens of cataract patients and have been proved as potential diagnostic biomarkers or therapeutic targets for cataracts. This review summarizes the study of relationship between the lens and ncRNAs, which can provide a novel insight into the pathogenesis of cataract.

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MiR-30a inhibits BECN1-mediated autophagy in diabetic cataract

Cited by 35 publications

References 44 publications

miR‐23b‐3p regulates apoptosis and autophagy via suppressing SIRT1 in lens epithelial cells

miR‐23b‐3p regulates apoptosis and autophagy via suppressing SIRT1 in lens epithelial cells

TRPM3_miR-204: a complex locus for eye development and disease

The Emerging Roles of Non-Coding RNAs in Cataract

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