LncRNA SND1-IT1 is involved in rat myocardial ischemia/reperfusion injury via regulating miR-183-5p

Xu, Xingshun; Ma, Shilun; Liu, Yancai

doi:10.23736/s0031-0808.20.03905-1

Cited by 4 publications

(3 citation statements)

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“…1,2 Its incidence is higher in middle-aged and elderly individuals, particularly in those with coronary artery disease and disorders that lead to heart failure, cardiac arrest, and sudden death. 3 Myocardial ischemia is a common complication of heart disease, and although specific therapies improve the blood flow to the injured myocardial tissues and can reduce mortality resulting from myocardial ischemia, reperfusion can cause other disorders such as reperfusion arrhythmias. 4 In traditional Chinese medicine, ginseng is considered to be the most important of all herbs and has great medical value.…”

Section: R E T R a C T E D Introductionmentioning

confidence: 99%

RETRACTED: Protective action of the ginsenoside Rh3 in a rat myocardial ischemia-reperfusion injury model by inhibition of apoptosis induced via p38 mitogen-activated protein kinase/caspase-3 signaling

et al. 2020

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Objective To investigate the protective effects of the ginsenoside Rh3 on rats subjected to myocardial ischemia-reperfusion (MIR) via its impact on caspase-3 and the p38 mitogen-activated protein kinase (MAPK) pathway. Methods Fifteen male Sprague-Dawley rats were randomly categorized into the MIR group (MY group, n = 5), sham surgery group (SS group, n = 5), and ginsenoside Rh3 group (GR group, n = 5). Results The MY group exhibited the largest myocardial infarctions compared with the GR and SS groups. The GR group exhibited significantly higher cell viability of cardiomyocytes and significantly decreased apoptosis compared with the MY group. Fibrils of infarcted tissue in the GR group were disordered but less swollen, with a more organized fibril orientation than those in the MY group. The GR group showed reduced p-p38 MAPK protein and caspase-3 mRNA expression levels compared with the MY and SS groups. Conclusions Rh3 significantly improved myocardial necrosis and caspase-3 levels in myocardial tissues by suppressing the p38 MAPK pathway, thereby inhibiting caspase-3 involvement in apoptosis. Thus, Rh3 was effective in inhibiting the escalated apoptotic pathway in myocardial infarction and can potentially serve as a useful therapeutic agent to rescue myocardial infarction.

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Section: R E T R a C T E D Introductionmentioning

confidence: 99%

RETRACTED: Protective action of the ginsenoside Rh3 in a rat myocardial ischemia-reperfusion injury model by inhibition of apoptosis induced via p38 mitogen-activated protein kinase/caspase-3 signaling

et al. 2020

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“…For instance, SND1-IT1 accelerates the proliferation and migration of osteosarcoma via sponging miR-665 to up-regulate POU2F1 expression [18]. In addition, SND1-IT1 is involved in rat myocardial ischemia/reperfusion injury via regulating miR-183-5p [37].…”

Section: Discussionmentioning

confidence: 99%

Exosome-mediated lncRNA SND1-IT1 from gastric cancer cells enhances malignant transformation of gastric mucosa cells via up-regulating SNAIL1

et al. 2022

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Background Gastric cancer (GC), as one of the most common malignancies across the globe, is the fourth leading cause of cancer-related deaths. Though a large body of research has been conducted to develop the therapeutic methods of GC, the survival rate of advanced patients is still poor. We aimed to dig into the potential regulatory mechanism of GC progression. Methods Bioinformatics tools and fundamental assays were performed at first to confirm the candidate genes in our study. The functional assays and mechanism experiments were conducted to verify the regulatory mechanisms of the genes underlying GC progression. Results Long non-coding RNA (lncRNA) SND1 intronic transcript 1 (SND1-IT1) is highly expressed in exosomes secreted by GC cells. SND1-IT1 was verified to bind to microRNA-1245b-5p (miR-1245b-5p) through competitive adsorption to promote ubiquitin specific protease 3 (USP3) messenger RNA (mRNA) expression. SND1-IT1 was validated to recruit DEAD-box helicase 54 (DDX54) to promote USP3 mRNA stability. SND1-IT1 induces malignant transformation of GES-1 cells through USP3. USP3 mediates the deubiquitination of snail family transcriptional repressor 1 (SNAIL1). Conclusions Exosome-mediated lncRNA SND1-IT1 from GC cells enhances malignant transformation of GES-1 cells via up-regulating SNAIL1. Graphical Abstract

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“…Inconsistent with Yang et al's findings, Zhang et al 47 demonstrated that epigallocatechin gallate, a myocardial injury protective agent, upregulated exosomal miR‐30a to inhibit autophagy and apoptosis in acute MI (AMI). Xu et al 48 also found that exosomal miR‐30a reduced cardiomyocyte apoptosis by inhibiting autophagy in rats with myocardial ischaemia/reperfusion (I/R) injury, which was not consistent with Yang's results, either. Autophagy is acutely activated during hypoxia, where it elicits a protective response, thereby mediating cellular adaptation and survival.…”

Section: Regulation Of Autophagy By Exosomesmentioning

confidence: 76%

Crosstalk between exosomes and autophagy: A review of molecular mechanisms and therapies

Xing

Tan

Miao

et al. 2021

J Cellular Molecular Medi

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Exosomes are extracellular vesicles that primarily exist in bodily fluids such as blood. Autophagy is an intracellular degradation process, which, along with exosomes, can significantly influence human health and has therefore attracted considerable attention in recent years. Exosomes have been shown to regulate the intracellular autophagic process, which, in turn, affects the circulating exosomes. However, crosstalk between exosomal and autophagic pathways is highly complex, depends primarily on the environment, and varies greatly in different diseases. In addition, studies have demonstrated that exosomes, from specific cell, can mitigate several diseases by regulating autophagy, which can also affect the excessive release of some harmful exosomes. This phenomenon lays a theoretical foundation for the improvement of many diseases. Herein, we review the mechanisms and clinical significance of the association and regulation of exosomes and autophagy, in order to provide a new perspective for the prevention and treatment of associated diseases.

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LncRNA SND1-IT1 is involved in rat myocardial ischemia/reperfusion injury via regulating miR-183-5p

Cited by 4 publications

References 0 publications

RETRACTED: Protective action of the ginsenoside Rh3 in a rat myocardial ischemia-reperfusion injury model by inhibition of apoptosis induced via p38 mitogen-activated protein kinase/caspase-3 signaling

RETRACTED: Protective action of the ginsenoside Rh3 in a rat myocardial ischemia-reperfusion injury model by inhibition of apoptosis induced via p38 mitogen-activated protein kinase/caspase-3 signaling

Exosome-mediated lncRNA SND1-IT1 from gastric cancer cells enhances malignant transformation of gastric mucosa cells via up-regulating SNAIL1

Crosstalk between exosomes and autophagy: A review of molecular mechanisms and therapies

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