Decoy receptor‑3 regulates inflammation and apoptosis via PI3K/AKT signaling pathway in coronary heart disease

Chen, Xinjing; Wang, Rehua; Chen, Wei; Lai, Li; Li, Zhiliang

doi:10.3892/etm.2019.7222

Cited by 18 publications

(20 citation statements)

References 52 publications

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“…In order to rescue myocardial apoptosis in STZ rat hearts, (Pro)renin receptor has been shown to inhibit apoptosis, and inflammatory response in rats with diabetic cardiomyopathy via extracellular signal-regulated kinase/ROS pathway (Dong et al, 2019). Decoy receptor-3 has been recently shown to regulate apoptosis via PI3K/AKT signaling pathway (Chen et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Electrical Conduction System Remodeling in Streptozotocin-Induced Diabetes Mellitus Rat Heart

et al. 2019

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Cardiovascular complications are common in type 1 diabetes mellitus (TIDM) and there is an increased risk of arrhythmias as a result of dysfunction of the cardiac conduction system (CCS). We have previously shown that, in vivo , there is a decrease in the heart rate and prolongation of the QRS complex in streptozotocin-induced type 1 diabetic rats indicating dysfunction of the CCS. The aim of this study was to investigate the function of the ex vivo CCS and key proteins that are involved in pacemaker mechanisms in TIDM. RR interval, PR interval and QRS complex duration were significantly increased in diabetic rats. The beating rate of the isolated sinoatrial node (SAN) preparation was significantly decreased in diabetic rats. The funny current density and cell capacitance were significantly decreased in diabetic nodal cells. Western blot showed that proteins involved in the function of the CCS were significantly decreased in diabetic rats, namely: HCN4, Ca v 1.3, Ca v 3.1, Cx45, and NCX1 in the SAN; RyR2 and NCX1 in the atrioventricular junction and Cx40, Cx43, Cx45, and RyR2 in the Purkinje network. We conclude that there are complex functional and cellular changes in the CCS in TIDM. The changes in the proteins involved in the function of this electrical system are expected to adversely affect action potential generation and propagation, and these changes are likely to be arrhythmogenic.

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Section: Discussionmentioning

confidence: 99%

Electrical Conduction System Remodeling in Streptozotocin-Induced Diabetes Mellitus Rat Heart

et al. 2019

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“…The restoration of myocardial blood supply is an important therapeutic strategy for AMI recovery ( 39 ). Therefore, the extent of angiogenesis mediated by vascular endothelial cells has become an important indicator for evaluating the prognosis of AMI ( 43 ).…”

Section: Discussionmentioning

confidence: 99%

miR‑124 promotes apoptosis and inhibits the proliferation of vessel endothelial cells through P38/MAPK and PI3K/AKT pathways, making it a potential mechanism of vessel endothelial injury in acute myocardial infarction

Ma¹,

Zhang²,

Liu³

2021

Exp Ther Med

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Due to its rapid onset and high rates of fatality, acute myocardial infarction (AMI) has long been one of the most fatal diseases among all types of heart diseases. Therefore, intensive research efforts have been focused on understanding AMI's potential pathogenesis to seek effective treatment options. In the present study, 20 peripheral blood samples were collected from patients with AMI, after which reverse transcription-quantitative PCR analysis revealed that microRNA (miR)-124 levels in the peripheral blood of patients with AMI was significantly elevated compared with that in the control group. In vitro , a model using pcDNA3.1-miR-124 transfected human umbilical vein endothelial cells (HUVECs) indicated that overexpression of miR-124 could significantly promote the apoptosis and suppress the proliferation of HUVECs using flow cytometry, TUNEL assay and Cell Counting Kit-8 assays. Based on the present findings, RNA samples of HUVECs overexpressing miR-124 was extracted and sequenced to explore the gene expression profile after miR-124 overexpression. Gene Set Enrichment Analysis (GSEA) analysis revealed that the downregulated genes were mainly enriched in signaling pathways, such as PI3K-AKT, whilst the upregulated genes were mainly enriched in metabolism-related signaling pathways, such as the metabolism of xenobiotics by cytochrome P450 pathway. Additionally, Rideogram software was used to determine the chromosomal localization of the differentially expressed genes. The results demonstrated that they were distributed on all chromosomes except for chromosome Y. In addition, characteristic profiles of the differentially expressed genes caused by miR-124 overexpression were analyzed using Connectivity Map. In total, two medicines, anisomycin and sanguinarine, which function as p38/MAPK signaling agonists that can inhibit angiogenesis, presented with the highest enrichment scores. Together with the GSEA results, which indicated that the differentially expressed genes were mainly enriched in the angiogenesis-inhibiting PI3K/AKT signaling pathway, the present study reported that high expression of miR-124 was negatively associated with patients with AMI, promoting the apoptosis and suppressing the proliferation of vessel endothelial cells.

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“…Herb-pharmacological activities, herb-compound, and compound-target relations were presented by the online Traditional Chinese Medicine Systems Pharmacology (TCMSP) database, and the analysis platform ( , accessed on 12 May 2021) [ 14 , 15 , 16 , 17 ]. The relationship between disease and Ilicis Purpureae Folium is shown in Figure S1 .…”

Section: Methodsmentioning

confidence: 99%

Kaempferol-3-O-Glucuronide Ameliorates Non-Alcoholic Steatohepatitis in High-Cholesterol-Diet-Induced Larval Zebrafish and HepG2 Cell Models via Regulating Oxidation Stress

Deng

Weng

et al. 2021

Life

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NAFLD (non-alcoholic fatty liver disease) is one of the most prominent liver diseases in the world. As a metabolic-related disease, the development of NAFLD is closely associated with various degrees of lipid accumulation, oxidation, inflammation, and fibrosis. Ilex chinensis Sims is a form of traditional Chinese medicine which is used to treat bronchitis, burns, pneumonia, ulceration, and chilblains. Kaempferol-3-O-glucuronide (K3O) is a natural chemical present in Ilex chinensis Sims. This study was designed to investigate the antioxidative, fat metabolism-regulating, and anti-inflammatory potential of K3O. A high-cholesterol diet (HCD) was used to establish steatosis in larval zebrafish, whereby 1mM free fatty acid (FFA) was used to induce lipid accumulation in HepG2 cells, while H2O2 was used to induce oxidative stress in HepG2. The results of this experiment showed that K3O reduced lipid accumulation and the level of reactive oxygen species (ROS) both in vivo (K3O, 40μM) and in vitro (K3O, 20μM). Additionally, K3O (40μM) reduced neutrophil aggregation in vivo. K3O (20μM) also decreased the level of malondialdehyde (MDA) and significantly increased the level of glutathione peroxidase (GSH-px) in both the HCD-induced larval zebrafish model and H2O2-exposed HepG2 cells. In the mechanism study, keap1, nrf2, tnf-α, and il-6 mRNA were all significantly reversed by K3O (20μM) in zebrafish. Changes in Keap1 and Nrf2 mRNA expression were also detected in H2O2-exposed HepG2 cells after they were treated with K3O (20μM). In conclusion, K3O exhibited a reduction in oxidative stress and lipid peroxidation, and this may be related to the Nrf2/Keap1 pathway in the NAFLD larval zebrafish model.

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Decoy receptor‑3 regulates inflammation and apoptosis via PI3K/AKT signaling pathway in coronary heart disease

Cited by 18 publications

References 52 publications

Electrical Conduction System Remodeling in Streptozotocin-Induced Diabetes Mellitus Rat Heart

Electrical Conduction System Remodeling in Streptozotocin-Induced Diabetes Mellitus Rat Heart

miR‑124 promotes apoptosis and inhibits the proliferation of vessel endothelial cells through P38/MAPK and PI3K/AKT pathways, making it a potential mechanism of vessel endothelial injury in acute myocardial infarction

Kaempferol-3-O-Glucuronide Ameliorates Non-Alcoholic Steatohepatitis in High-Cholesterol-Diet-Induced Larval Zebrafish and HepG2 Cell Models via Regulating Oxidation Stress

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