Upregulation of miR-499a-5p Decreases Cerebral Ischemia/Reperfusion Injury by Targeting PDCD4

Shan, Weifeng; Ge, Huifeng; Chen, Bingquan; Zhu, Shu; Zhou, Yanfeng

doi:10.1007/s10571-021-01085-4

Cited by 11 publications

(8 citation statements)

References 35 publications

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“…PDCD4 facilitated lung tumor cell apoptosis by inhibiting p62-Nrf2 signaling pathway and up-regulating Keap1 expression ( 44 ). After the expression of PDCD4 was inhibited by miR-499a-5p, neuronal apoptosis decreased in ischemic brain injury ( 45 ). In this study, we found that miR-93-5p overexpression significantly reduced the expression of PDCD4, which inhibited the apoptosis of AOH retinal neurons ( Figs 2 – 4 ).…”

Section: Discussionmentioning

confidence: 99%

MiR-93-5p inhibits retinal neurons apoptosis by regulating PDCD4 in acute ocular hypertension model

Tan,

Shi,

Zhang

et al. 2023

Life Sci. Alliance

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The present study focused on the effect of miR-93-5p on apoptosis of retinal neurons in acute ocular hypertension (AOH) model by regulating PDCD4 and explored its related mechanism. We detected that miR-93-5p expression was decreased and PDCD4 expression was increased in the AOH retina by qRT-PCR. Therefore, we explored the role of miR-93-5p and PDCD4. MiR-93-5p overexpression inhibited the apoptosis of retinal neurons and the expression of PDCD4 in vivo and in vitro. Inhibiting the expression of PDCD4 via transfected interfering RNA decreased the apoptosis of retinal cells and increased the expression of PI3K/Akt pathway–related proteins in vitro. However, the addition of PI3K protein inhibitor LY294002 reversed this effect, leading to a decrease of PI3K/Akt pathway protein expression and an increase of apoptosis-related protein Bax/Bcl-2 expression ratio. Finally, up-regulating miR-93-5p or down-regulating PDCD4 increased the expression of PI3K/Akt pathway protein in vivo. In conclusion, under the condition of AOH injury, miR-93-5p-inhibiting PDCD4 expression reduced the apoptosis of retinal neurons by activating PI3K/Akt pathway.

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Section: Discussionmentioning

confidence: 99%

MiR-93-5p inhibits retinal neurons apoptosis by regulating PDCD4 in acute ocular hypertension model

Tan,

Shi,

Zhang

et al. 2023

Life Sci. Alliance

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“…Our result presented with elevated concentrations of CK-MB and BNP while the concentrations of SOD and COX IV were reduced in LPS-treated AC16 cells, whereas an overexpression of miR-499a-5p could invert the findings. Shan et al have implicated miR-499a-5p upregulation in the mitigation of cerebral I/R injury [ 37 ]. Similarly, our result elicited that miR-499a-5p overexpression alleviated SIMD.…”

Section: Discussionmentioning

confidence: 99%

Predictive value and regulatory mechanism of serum miR-499a-5p on myocardial dysfunction in sepsis

Yang

Wen

2021

J Cardiothorac Surg

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Background This study sought to investigate the predictive value and regulatory mechanism of serum miR-499a-5p in sepsis-induced myocardial dysfunction (SIMD). Methods A total of 60 patients with sepsis and 60 healthy volunteers were enrolled in this study. The serum levels of miRNAs (miR-451, miR-378 and miR-499a-5p) were detected. Receiver operating characteristic curve and logistic regression analysis were used to evaluate the diagnostic and prognostic value of miR-499a-5p in SIMD patients. AC16 cells were used to establish SIMD model in vitro using lipopolysaccharide (LPS). An analysis was conducted for miR-499a-5p expression, cell viability, and the concentration of creatine kinase-MB isoform (CK-MB), brain natriuretic peptide (BNP), superoxide dismutase (SOD) and cytochrome C oxidase IV (COX IV). The downstream target of miR-499a-5p was verified. Results Our results revealed a poor expression of miR-499a-5p in the serum of SIMD patients, while no significant difference was evident for miR-451 and miR-378. The level of miR-499a-5p in the survival group was higher than the non-survival group. miR-499a-5p elicited good diagnostic and prognostic value for SIMD. Our findings revealed that miR-499a-5p was decreased significantly in LPS-treated cardiomyocytes. After overexpression of miR-499a-5p, the cell viability increased, and the concentrations of CK-MB and BNP were decreased, while the concentrations of SOD and COX IV were increased. EIF4E was validated as the target of miR-499a-5p. After overexpression of EIF4E, the cell viability was decreased and the concentrations of CK-MB and BNP were increased while the concentrations of SOD and COX IV were decreased. Conclusion The level of miR-499a-5p is weak in SIMD patients. miR-499a-5p has a good diagnostic and prognostic value for SIMD by inhibiting EIF4E transcription.

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“…Existing studies have revealed that PDCD4 knockout can reduce the chronic stress-induced depression-like behavior in mice ( 14 ), whereas increased PDCD4 levels in vitro can lead to significant reductions in axonal length ( 15 ). In addition, PDCD4 knockdown has been observed to reduce infarct damage and cortical neuronal apoptosis induced by brain ischemia/reperfusion injury ( 16 ).…”

Section: Introductionmentioning

confidence: 99%

Programmed cell death 4 blocks autophagy and promotes dopaminergic neuronal injury in Parkinson's disease

Cao,

Kang,

et al. 2024

Exp Ther Med

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Dysregulation of autophagy has previously been associated with the formation of toxic proteins, such as α-synuclein, in patients with Parkinson's disease (PD). In addition, it has been indicated that programmed cell death 4 (PDCD4) can inhibit autophagy in certain conditions, such as diabetic nephropathy, atherosclerosis and cardiac hypertrophy. Therefore, the hypothesis that PDCD4 can promote dopaminergic neuron damage through autophagy was proposed. To explore this hypothesis, the present study treated human neuroblastoma SK-N-SH cells with 1-methyl-4-phenylpyridinium (MPP + ) to establish an in vitro model of PD. The potential effects of PDCD4 knockdown on lactate dehydrogenase (LDH) release, cell apoptosis, inflammatory response, oxidative stress and autophagy were then evaluated in this model of PD using an LDH assay kit, flow cytometry, western blotting, ELISA and immunofluorescence. The autophagy inhibitor 3-methyladenine (3-MA) was also applied to treat these cells, and its effects on these aforementioned parameters following PDCD4 knockdown were assessed. MPP + was shown to increase the expression levels of PDCD4 in SK-N-SH cells. PDCD4 knockdown was revealed to suppress LDH release, cell apoptosis, secretion of inflammatory factors and oxidative stress. In addition, PDCD4 knockdown was demonstrated to enhance autophagy in cells treated with MPP + . By contrast, 3-MA treatment reversed the aforementioned effects of PDCD4 knockdown on cells, suggesting autophagy to be among the processes regulated by PDCD4 in SK-N-SH cells. The results of the present study suggested the existence of regulatory effects mediated by PDCD4 on autophagy in MPP + -induced SK-N-SH cells, offering potential future targets for PD therapy.

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Upregulation of miR-499a-5p Decreases Cerebral Ischemia/Reperfusion Injury by Targeting PDCD4

Cited by 11 publications

References 35 publications

MiR-93-5p inhibits retinal neurons apoptosis by regulating PDCD4 in acute ocular hypertension model

MiR-93-5p inhibits retinal neurons apoptosis by regulating PDCD4 in acute ocular hypertension model

Predictive value and regulatory mechanism of serum miR-499a-5p on myocardial dysfunction in sepsis

Programmed cell death 4 blocks autophagy and promotes dopaminergic neuronal injury in Parkinson's disease

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