Overexpression of MicroRNA-122 Resists Oxidative Stress-Induced Human Umbilical Vascular Endothelial Cell Injury by Inhibition of p53

Li, Huaqing; Pan, Zhiyu; Yang, Zhen; Zhang, Don-Bing; Chen, Qian

doi:10.1155/2020/9791608

Cited by 9 publications

(9 citation statements)

References 27 publications

(27 reference statements)

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“…In order to explore the toxic effect of SMI on HUVECs, we pretreated HUVECs with SMI (0, 0.5%, 1%, 5%, 10%, 20%, 30%, 50%) for 12 h. Results of cell viability showed that the concentration of SMI should be less than 20%. Then, for selecting the most suitable concentration of intervention of SMI, we pretreated HUVECs with SMI (0, 1%, 2%, 2.5%, 3%, 4%, 5%) for 12 h and then treated with H 2 O 2 (0.6 mM) for 2 h to induce an endothelial cell injury model [ 18 , 19 ]. According to the test of cell viability, we decided to incubate HUVECs with SMI at the concentrations of 1% and 5% in the further study.…”

Section: Methodsmentioning

confidence: 99%

Pretreatment with Shenmai Injection Protects against Coronary Microvascular Dysfunction

Zheng

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Background. The clinical treatment of coronary microvascular dysfunction (CMD) is mainly based on conventional medicine, but the mechanism of the medicine is single and the efficacy is different. Shenmai injection (SMI) has a variety of ingredients, but the effect of SMI on CMD has not been studied. This study investigated the effect of SMI on CMD and its possible mechanism. Methods. The protective effect of SMI on CMD was evaluated in Sprague-Dawley (SD) rats and human umbilical vein endothelial cells (HUVECs). In vivo, forty-five male SD rats were randomly divided into control group (sham group), CMD group (model group), and SMI group (treatment group). Two weeks after SMI intervention, laurate was injected into the left ventricle of rats to construct a CMD model. Blood samples were collected to detect myocardial enzymes, oxidative stress, and inflammatory factors, and the hearts of rats were extracted for histopathological staining and western blot detection. In vitro, a hydrogen peroxide-induced endothelial injury model was established in HUVECs. After pretreatment with SMI, cell viability, oxidative stress, vasodilative factors, and apoptosis were detected. Results. In vivo, pretreatment with SMI could effectively reduce the concentrations of lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), cardiac troponin I (cTnI), endothelin-1 (ET-1), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), and malondialdehyde (MDA) in the serum of rats. Meanwhile, the expression of bcl-2-associated X (Bax) and caspase-3 protein in the myocardium of rats was decreased in the SMI group. The levels of nitric oxide (NO) and superoxide dismutase (SOD) and the expression of B-cell lymphoma-2 (Bcl-2) were higher in the SMI group than in the CMD group. Pathological staining results showed that SMI could effectively reduce inflammatory infiltration and the formation of collagen fibers and microthrombus in the rat myocardium. In vitro, intervention with SMI could improve endothelial function in a dose-dependent manner as evidenced by increasing the activity of endothelial cells and the expression of NO, SOD, endothelial nitric oxide synthase (eNOS), and Bcl-2, while decreasing cell apoptosis and the levels of ET-1, MDA, Bax, and caspase-3. Conclusions. Pretreatment with SMI could improve CMD by alleviating oxidative stress, inflammatory response, and apoptosis and then improving vascular endothelial function and microvascular structure.

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Section: Methodsmentioning

confidence: 99%

Pretreatment with Shenmai Injection Protects against Coronary Microvascular Dysfunction

Zheng

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…They accelerate injury and apoptosis of VECs and cause shape elongation, aggregation and cytoskeletal rearrangement of VECs, thereby promoting DVT formation. Previous studies have reported that miR-122 (82), miR-181a-5p (83), miR-195-5p (84), miR-206 (85), miR-338-5p (86), miR-383-5p (87), miR-448 (88), miR-483-3p (89), miR-525p-5p (90) and let-7e-5p (91) can act on their respective target proteins to promote DVT formation. These aforementioned studies suggest that miRNAs can promote the release of inflammatory factors and accelerate oxidative stress-mediated cellular injury, leading to the loss of barrier and material transport functions and exacerbation of ischemic and hypoxic damage to the vascular microenvironment.…”

Section: Mirnas In Endothelial Cells Regulate Dvtmentioning

confidence: 99%

Advances in microRNA regulation of deep vein thrombosis through venous vascular endothelial cells (Review)

Fang,

Huang,

Yao

et al. 2024

Mol Med Rep

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Deep vein thrombosis (DVT) is a prevalent clinical venous thrombotic condition that often manifests independently or in conjunction with other ailments. Thrombi have the propensity to dislodge into the circulatory system, giving rise to complications such as pulmonary embolism, thereby posing a significant risk to the patient. Virchow proposed that blood stagnation, alterations in the vessel wall and hypercoagulation are primary factors contributing to the development of venous thrombosis. Vascular endothelial cells (VECs) constitute the initial barrier to the vascular wall and are a focal point of ongoing research. These cells exert diverse stimulatory effects on the bloodstream and secrete various regulatory factors that uphold the dynamic equilibrium between the coagulation and anticoagulation processes. MicroRNAs (miRNAs) represent a class of non-coding RNAs present in eukaryotes, characterized by significant genetic and evolutionary conservation and displaying high spatiotemporal expression specificity. Typically ranging from 20 to 25 bases in length, miRNAs can influence downstream gene transcription through RNA interference or by binding to specific mRNA sites. Consequently, advancements in understanding the molecular mechanisms of miRNAs, including their functionalities, involve modulation of vascular-associated processes such as cell proliferation, differentiation, secretion of inflammatory factors, migration, apoptosis and vascular remodeling regeneration. miRNAs play a substantial role in DVT formation via venous VECs. In the present review, the distinct functions of various miRNAs in endothelial cells are outlined and recent progress in comprehending their role in the pathogenesis and clinical application of DVT is elucidated. Contents 1. Introduction 2. miRNAs in endothelial cells regulate DVT 3. Clinical application of miRNAs in DVT 4. Conclusions and future perspectives

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“…MicroRNAs (miRNAs) are the class of evolutionarily conserved noncoding RNAs with the function of regulating gene expression at the translational level 25,26 . MiRNAs were reported to play important roles in development of DVT, and lncRNAs were involved in regulation of DVT as competitive RNAs (ceRNAs) for miRNAs 13,22,27–29 . Study has shown that GUSBP5‐AS regulates angiogenesis and proliferation of EPCs through miR‐223‐3p, and alleviates development of DVT 30 .…”

Section: Introductionmentioning

confidence: 99%

“… 25 , 26 MiRNAs were reported to play important roles in development of DVT, and lncRNAs were involved in regulation of DVT as competitive RNAs (ceRNAs) for miRNAs. 13 , 22 , 27 , 28 , 29 Study has shown that GUSBP5‐AS regulates angiogenesis and proliferation of EPCs through miR‐223‐3p, and alleviates development of DVT. 30 In addition, downregulation of LINC01123 inhibited DVT formation via miRNA‐125a‐3p.…”

Section: Introductionmentioning

confidence: 99%

By modulating miR‐525‐5p/Bax axis, LINC00659 promotes vascular endothelial cell apoptosis

Zhu

Chen

2023

Immunity Inflam & Disease

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Background Deep vein thrombosis (DVT) is a vascular disease that has no effective treatment at present. Endothelial cells play a crucial role in the processes vasoconstriction, platelet activation, and blood coagulation and are an integral part of the vascular response to injury resulting in thrombus formation. Objective The aim of this study was to investigate the roles and mechanisms of long noncoding RNA LINC00659 (LINC00659) in endothelial cells. Methods The functions of LINC00659 and miR‐525‐5p on endothelial cells were explored by cell transfection assays, and the expression levels of LINC00659, miR‐525‐5p, and Bax in human umbilical vein endothelial cells (HUVECs) were assessed with reverse transcriptase‐quantitative polymerase chain reaction (RT‐qPCR). Binding sites of LINC00659 and miR‐525‐5p were subsequently analyzed with bioinformatics software, and validated with dual‐luciferase reporter gene assay. Effects of LINC00659 and miR‐525‐5p on proliferation and apoptosis of HUVECs were detected with MTT (3‐(45)‐dimethylthiahiazo (‐z‐y1)‐35‐di‐phenytetrazoliumromide) assay and flow cytometry. RT‐qPCR and western blot analysis were used to evaluate the mRNA and protein levels of apoptosis‐related markers Bcl‐2 and Bax in HUVECs. Results LINC00659 directly targeted and negatively regulated miR‐525‐5p, and Bax was a target of miR‐525‐5p. Upregulation of LINC00659 could inhibit proliferation and promote apoptosis of HUVECs, while the silencing of LINC00659 could increase the viability of HUVECs and inhibit apoptosis via upregulating miR‐525‐5p. Further mechanistic studies revealed miR‐525‐5p could negatively regulate Bax in HUVECs, and increased the viability of HUVECs and inhibited apoptosis by downregulating Bax expression. Conclusion LINC00659 played an important role in DVT by regulating the apoptosis of vascular endothelial cells through regulating miR‐525‐5p/Bax axis.

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Overexpression of MicroRNA-122 Resists Oxidative Stress-Induced Human Umbilical Vascular Endothelial Cell Injury by Inhibition of p53

Cited by 9 publications

References 27 publications

Pretreatment with Shenmai Injection Protects against Coronary Microvascular Dysfunction

Pretreatment with Shenmai Injection Protects against Coronary Microvascular Dysfunction

Advances in microRNA regulation of deep vein thrombosis through venous vascular endothelial cells (Review)

By modulating miR‐525‐5p/Bax axis, LINC00659 promotes vascular endothelial cell apoptosis

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