miR-24-p53 pathway evoked by oxidative stress promotes lens epithelial cell apoptosis in age-related cataracts

Lü, Bo; Christensen, Ian T.; Ma, Liwei; Wang, Xin‐Ling; Jiang, Linfeng; Wang, Chunxia; Li, Feng; Zhang, Jinsong; Yan, Qichang

doi:10.3892/mmr.2018.8492

Cited by 17 publications

(17 citation statements)

References 41 publications

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“…Abnormal miRNAs expressions have also been implicated in cataracts. Lu et al reported that the expression of miR‐24 was significantly increased in human anterior lens capsules of age associated cataracts and lens epithelial cells exposed to oxidative stress . Lu and colleagues described that miR‐211 was highly expressed in anterior lens capsules of patients with age‐related cataracts .…”

Section: Discussionmentioning

confidence: 99%

Retracted: MicroRNA‐4328 promotes lens epithelial cell apoptosis by targeting NLR family, apoptosis inhibitory protein in age‐related cataract

Zhu

Gong²,

Zhao

2019

Cell Biochemistry & Function

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Cataract is the leading cause of blindness in the world while the molecular mechanisms of cataracts pathogenesis are not well elucidated. Dysregulated microRNA (miRNA) expressions have been implicated in cataract. However, the precise role of miR-4328 in cataract is still unknown. We compared the expression level of total miR-4328 between clinical samples from healthy people and cataract patient and between UV-irradiated and control lens epithelial cells. We determined the effect of miR-4328 on lens epithelial cell proliferation and apoptosis by suppressing miR-4328. We further predicted NLR Family Apoptosis Inhibitory Protein (NAIP) as potential target of miR-4328 and continued to evaluate the effects of NAIP on cell proliferation and apoptosis. MiR-4328 was up-regulated in cataract sample and in UVirradiated lens epithelial cells. Suppressing MiR-4328 promoted cell proliferation and inhibited apoptosis. MiR-4328 targeted NAIP and suppressed its expression. Knocking down NAIP abolished the effects of miR-4328 on cell proliferation and inhibited apoptosis. MiR-4328 promotes lens epithelial cell apoptosis by targeting NAIP in age-related cataract. Significance of the study: MiR-4328 targeted NAIP and suppressed its expression. Knocking down NAIP abolished the effects of miR-4328 on cell proliferation and inhibited apoptosis. MiR-4328 promotes lens epithelial cell apoptosis by targeting NAIP in age-related cataract.

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Section: Discussionmentioning

confidence: 99%

Retracted: MicroRNA‐4328 promotes lens epithelial cell apoptosis by targeting NLR family, apoptosis inhibitory protein in age‐related cataract

Zhu

Gong²,

Zhao

2019

Cell Biochemistry & Function

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“…MiR‐24 plays important role in inflammation, cell migration and many diseases. Moreover, it was shown that oxidative stress leads to up‐regulation of miR‐24 an in consequence to apoptosis . On the other hand, miR‐519 was shown to block autophagy .…”

Section: Introductionmentioning

confidence: 99%

5‐Azacytydine and resveratrol reverse senescence and ageing of adipose stem cells via modulation of mitochondrial dynamics and autophagy

Kornicka

Szłapka-Kosarzewska

Śmieszek

et al. 2018

J Cellular Molecular Medi

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Obesity and endocrine disorders have become prevalent issues in the field of both human and veterinary medicine. Equine metabolic syndrome is a complex disorder involving alternation in metabolism and chronic systemic inflammation. It has been shown that unfavourable microenvironment of inflamed adipose tissue negatively affects adipose stem cell population (ASC) residing within, markedly limiting their therapeutic potential. ASCsEMS are characterized by increased senescence apoptosis, excessive accumulation of reactive oxygen species (ROS), mitochondria deterioration and “autophagic flux.” The aim of the present study was to evaluate whether treatment of ASCsEMS with a combination of 5‐azacytydine (AZA) and resveratrol (RES) would reverse aged phenotype of these cells. For this reason, we performed the following analyzes: molecular biology (RT‐PCR), microscopic (immunofluorescence, TEM) and flow cytometry (JC‐1, ROS, Ki67). We evaluated the mitochondrial status, dynamics and clearance as well as autophagic pathways. Furthermore, we investigated epigenetic alternations in treated cells by measuring the expression of TET genes and analysis of DNA methylation status. We have demonstrated that AZA/RES treatment of ASCsEMS is able to rejuvenate these cells by modulating mitochondrial dynamics, in particular by promoting mitochondrial fusion over fission. After AZA/RES treatment, ASCsEMS were characterized by increased proliferation rate, decreased apoptosis and senescence and lower ROS accumulation. Our findings offer a novel approach and potential targets for the beneficial effects of AZA/RES in ameliorating stem cell dysfunctions.

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“…The results showed that the mRNA and protein expression level of SIRT1 in group C were significantly lower than those in group A and B, while the P53 level in group C was higher than those in group A and B, and the level of apoptosis was also significantly higher than those in group A and B. Kondo et al (21) found in animal models that SIRT1 could regulate eye aging and protect eye tissues from oxidative stress, and the increase in its level could prevent age-related cataracts. In the study of Lu et al (22), it was pointed out that P53 was at a higher level in age-related cataracts and could aggravate cataracts through increasing the apoptosis of lens epithelial cells. Zheng and Lu (23) demonstrated that the expression of SIRT1 could increase when P53 was suppressed.…”

Section: Discussionmentioning

confidence: 99%

Expression of miR‑34a in cataract rats and its related mechanism

2019

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Expression of miR-34a in cataract rats and its related mechanism were investigated. A total of 30 SD rats were selected and divided into three groups: group A: 2-month-old lucent lens, group B: 18-month-old lucent lens, and group C: 18-month-old naturally occurring cataract lens. The lens was taken and measured by LOC III to determine the degree of lens opacity of the three groups of rats. qPCR was used to detect expression of miR-34a and mRNA of SIRT1 and P53. Western blotting was used to detect the protein expression of SIRT1 and P53. Cell apoptosis was detected by flow cytometry. The lens of rats in group C was more turbid than that of groups A and B (P<0.05). The expression levels of miR-34a and P53 mRNA in the rats lens of group C were significantly higher than those in groups A and B, and the expression of SIRT1 mRNA was significantly lower than that of groups A and group B (P<0.05). Expression of miR-34a in group A was significantly higher than that in group B, the mRNA expression of SIRT1 was significantly lower than that in the lucent lens of 18-month-old rats (P<0.05). The expression of SIRT1 protein in group C was significantly lower than that in groups A and group B, while the expression level of P53 protein in group C was significantly higher than that of groups A and B. The expression of SIRT1 protein in group B was significantly higher than that in group A (P<0.05). The apoptosis rate of group C was higher than that of groups A and group B (P<0.05). In conclusion, the upregulation of expression level of miR-34a is related to cataract occurrence in rats, which may be caused by regulation of SIRT1 protein.

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miR-24-p53 pathway evoked by oxidative stress promotes lens epithelial cell apoptosis in age-related cataracts

Cited by 17 publications

References 41 publications

Retracted: MicroRNA‐4328 promotes lens epithelial cell apoptosis by targeting NLR family, apoptosis inhibitory protein in age‐related cataract

Retracted: MicroRNA‐4328 promotes lens epithelial cell apoptosis by targeting NLR family, apoptosis inhibitory protein in age‐related cataract

5‐Azacytydine and resveratrol reverse senescence and ageing of adipose stem cells via modulation of mitochondrial dynamics and autophagy

Expression of miR‑34a in cataract rats and its related mechanism

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