MicroRNA‑146b induces the PI3K/Akt/NF‑κB signaling pathway to reduce vascular�inflammation and apoptosis in myocardial infarction by targeting PTEN

“…Sprouty homolog 1 is located on chromosome 4 of human beings and has been reported to participate in the regulation of various cell functions [34]. In addition, SPRY1 has been reported to regulate neuronal apoptosis [22,35] and predicted as the potential downstream target of miR-187 by using the TargetScan software, which indicated that miR-187 might alleviate PTZ-induced epilepsy in rats by targeting SPRY1. However, there are still no literature reports of a role of SPRY1 in the development of epilepsy.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-187 inhibits pentylenetetrazol-induced neuronal apoptosis and alleviates development of epilepsy in epileptic rats by regulating SPRY1 expression

Diao¹,

Yu²,

Wang³

et al. 2021

Trop. J. Pharm Res

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Purpose: To explore the role of microRNA-187 on the pathological process of epilepsy. Methods: The seizure score of epileptic rats was evaluated according to Racine’s scale. Real-time quantitative polymerase chain reaction (RT-qPCR) was performed to determine the expression levels of microRNA-187 (miR-187). Western blot technique was conducted to assess the expression levels of caspase 3, B-cell lymphoma-2 (BCL-2), and poly (ADP-ribose) polymerase (PARP)] and activation of phosphatase and tensin homolog (PTEN)/PI3K/AKT cascade. Caspase 3 colorimetric assay kit was employed to evaluate the activity of caspase 3. Dual-luciferase reporter gene system was used to explore the regulating mechanisms of miR-187 and protein sprouty homolog 1 gene (SPRY1). Results: The results showed that miR-187 was aberrantly downregulated in the hippocampus regions of pentylenetetrazol (PTZ)-treated rats compared to normal rats (p < 0.05). Furthermore, PTZ promoted caspase 3-dependent neuronal apoptosis by increasing the expression of pro-apoptosis protein PARP and decreasing the expression levels of BCL-2 in rats. On the other hand, overexpression of miR-187 downregulated SPRY1 as well as PTEN (p < 0.05), thereby activating the downstream PI3K/AKT signaling pathway. Notably, the effects of upregulated miR-187 on neuronal apoptosis and epilepsy development in PTZ-induced rats was reversed by the concomitant overexpression of SPRY1 (p < 0.05). Conclusion: The results of this research show that overexpressed miR-187 alleviates the development of PTZ-induced neuronal apoptosis and epilepsy in epileptic rat models by regulating SPRY1 expression. These findings can hopefully be beneficial for the discovery of new therapeutic strategies for epilepsy treatment.

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“…They also reduced ETS-1 expression and cell hypertrophy. Previous studies suggested that miRNA-regulated cytokine production is mediated by modulating AKT/NF-κB ( Zhao et al, 2019 ). miRNA-29a regulates lipopolysaccharide-induced inflammatory responses in murine macrophages through the Akt1/NF-κB pathway ( Tang et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-221/222 Mediates ADSC-Exosome-Induced Cardioprotection Against Ischemia/Reperfusion by Targeting PUMA and ETS-1

Lai

Lee

Chang

et al. 2020

Front. Cell Dev. Biol.

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Cardiovascular disease is a major health problem in industrialized and developing countries and is the leading cause of death and disability. Myocardial ischemia/reperfusion (I/R) causes cardiomyocyte damage such as apoptosis and hypertrophy. The purpose of this study was to investigate the effects of exosomes from adipose-derived stem cells (ADSC-Exo) on hearts from I/R mice and to explore the underlying mechanisms. ADSC-Exo significantly decreased I/R-induced cardiomyocyte apoptosis and hypertrophy, as detected by TdT-mediated dUTP nick end-labeling (TUNEL) and wheat germ agglutinin (WGA) staining, respectively. In addition, the expression of apoptosis-related proteins p-p53 and PUMA and hypertrophy-related proteins ETS-1 and ANP were significantly reduced in the cardiomyocytes of ADSC-Exo-treated I/R mice compared to those of control mice. Both PUMA and ETS-1 are reported to be target genes for miR-221/222. I/R operation significantly reduced miR-221/222 expression, while ADSC-Exo treatment increased miR-221/222 expression, as detected by RT-qPCR. We also observed that cardiac I/R operation markedly increased cell apoptosis and hypertrophy in miR-221/222 knockout (KO) mice, while ADSC-Exo reduced the effects of I/R operation. Furthermore, ADSC-Exo protected H9c2 cardiomyocytes from H2O2-induced damage by reducing apoptosis and hypertrophy in vitro. H2O2 treatment significantly reduced miR-221/222 expression, while ADSC-Exo treatment reversed this effect in H9c2 cells. ADSC-Exo treatment decreased H2O2-induced PUMA and ETS-1 expression. Compared with control treatment, I/R treatment significantly reduced p-AKT and increased p-p65, while ADSC-Exo and miR-221/222 mimics attenuated these effects. The AKT activator SC79 and p65 inhibitor Bay 11-7082 reduced H2O2-induced cell apoptosis and hypertrophy. Based on these findings, ADSC-Exo prevents cardiac I/R injury through the miR-221/miR-222/PUMA/ETS-1 pathway. Therefore, ADSC-Exo is an effective inhibitor of I/R-induced heart injury.

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MicroRNA‑146b induces the PI3K/Akt/NF‑κB signaling pathway to reduce vascular�inflammation and apoptosis in myocardial infarction by targeting PTEN

Cited by 21 publications

References 27 publications

Protective effect of Qingre Huoxue decoction against myocardial infarction via PI3K/Akt autophagy pathway based on UPLC-MS, network pharmacology, and in vivo evidence

Protective effect of Qingre Huoxue decoction against myocardial infarction via PI3K/Akt autophagy pathway based on UPLC-MS, network pharmacology, and in vivo evidence

MicroRNA-187 inhibits pentylenetetrazol-induced neuronal apoptosis and alleviates development of epilepsy in epileptic rats by regulating SPRY1 expression

MicroRNA-221/222 Mediates ADSC-Exosome-Induced Cardioprotection Against Ischemia/Reperfusion by Targeting PUMA and ETS-1

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