miR-503/Apelin-12 mediates high glucose-induced microvascular endothelial cells injury via JNK and p38MAPK signaling pathway

Chen, Kai; Zhao, Xin-Lan; Lang-Bo, Li; Huang, Lingyun; Tang, Zhuo; Luo, Juan; Yang, Li; Qin, Aiping; Hu, Fang

doi:10.1016/j.reth.2019.12.002

Cited by 19 publications

(27 citation statements)

References 40 publications

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“…miR-503 overexpression increased podocytes apoptosis, while its inhibition improved renal function in rats of Diabetes mellitus via targeting E2F3 ( Zha et al, 2019 ). In human microvascular endothelial cells (HMEC-1) ( Chen et al, 2020 ), HG treatment also increased miR-503 expression level markedly, but decreased the expression of Apelin-12, which was proven to be a miR-503 target by luciferase assay. miR-503 inhibited Apelin-12 expression, while it up-regulated the phosphorylation of JNK and p38MAPK.…”

Section: Introductionmentioning

confidence: 99%

“…miR-503 inhibited Apelin-12 expression, while it up-regulated the phosphorylation of JNK and p38MAPK. In contrast, inhibition of miR-503 alleviated oxidative stress, inflammation and apoptosis induced by HG in HMEC-1 cells ( Chen et al, 2020 ). The expression level of miR-503 induced by HG in both types of cells is consistent, and the increase of miR-503 contributes to cell apoptosis under HG condition.…”

Section: Introductionmentioning

confidence: 99%

“…By contrast, miR-7 can target Keap1 and activate Nrf2 pathway, therefore, it can relieve oxidative stress and exert cytoprotective effects by regulating the Nrf2 pathway ( Kabaria et al, 2015 ). Several studies have reported that miR-503 is involved in oxidative stress ( Miao et al, 2017 ; Rubattu et al, 2017 ; Chen et al, 2020 ; Zhang et al, 2020 ). In this section, we summarize and analyze the mechanisms of miR-503 in oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

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The Causes and Consequences of miR-503 Dysregulation and Its Impact on Cardiovascular Disease and Cancer

Cai

Pai

et al. 2021

Front. Pharmacol.

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microRNAs (miRs) are short, non-coding RNAs that regulate gene expression by mRNA degradation or translational repression. Accumulated studies have demonstrated that miRs participate in various biological processes including cell differentiation, proliferation, apoptosis, metabolism and development, and the dysregulation of miRs expression are involved in different human diseases, such as neurological, cardiovascular disease and cancer. microRNA-503 (miR-503), one member of miR-16 family, has been studied widely in cardiovascular disease and cancer. In this review, we summarize and discuss the studies of miR-503 in vitro and in vivo, and how miR-503 regulates gene expression from different aspects of pathological processes of diseases, including carcinogenesis, angiogenesis, tissue fibrosis and oxidative stress; We will also discuss the mechanisms of dysregulation of miR-503, and whether miR-503 could be applied as a diagnostic marker or therapeutic target in cardiovascular disease or cancer.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The Causes and Consequences of miR-503 Dysregulation and Its Impact on Cardiovascular Disease and Cancer

Cai

Pai

et al. 2021

Front. Pharmacol.

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“…12 In HG-induced microvascular cells injury, miR-503/Apelin-12 enhanced inflammation and oxidative stress by regulating JNK and p38MAPK pathway, suggesting a potential therapeutic target for diabetic angiopathy (DA). 13 Zha et al reported for the first time that miR-503 was highly expressed in podocytes treated with high glucose in vitro and diabetic rat kidney tissues, inhibiting E2F transcription factor 3 (E2F3), promoting podocyte apoptosis, and participating in the pathological mechanism of DN. 14 Targetscan software predicted that Bcl-2 was the direct target of miR-503.…”

Section: Introductionmentioning

confidence: 99%

<p>LncRNA MIR503HG Promotes High-Glucose-Induced Proximal Tubular Cell Apoptosis by Targeting miR-503-5p/Bcl-2 Pathway</p>

Cao¹,

Fan²

2020

DMSO

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Aim: More than half of microRNAs are located in genes. LncRNAs are host genes of intronic microRNAs that regulate intracellular splicing to form pre-miRNAs that are processed to mature miRNAs. MicroRNAs work as partners or antagonists of their host lncRNAs by fine-tuning their target genes. However, whether lncRNA-MIR503HG (miR-503 host gene) is co-transcribed with miR-503 and affects miR-503 splicing, thereby affecting its target gene Bcl-2 expression and cell mitochondrial apoptotic pathway in diabetic nephropathy (DN) is currently unknown. Methods: Human proximal tubular (HK-2) cells cultured in high glucose were transfected with lncRNA MIR503HG overexpression/inhibition plasmid and miR-503 mimics/inhibitor. Real-time quantitative PCR was used to measure the expression levels of lncRNA MIR503HG, pre-miR-503, miR-503 and Bcl-2. Western blot was used to measure the protein expressions of Bcl-2, Bax, Cytc and cleaved-caspase 9/3. Annexin V/PI flow cytometry was used to measure apoptosis. Results: Host lncRNA MIR503HG was co-transcribed with miR-503. MIR503HG regulated the expression of miR-503 by affecting miR-503 splicing synthesis. In the presence of high glucose, the expression levels of lncRNA MIR503HG and miR-503 were up-regulated in HK-2 cells cultured in high glucose. Bcl-2 expression was inhibited and levels of apoptosisrelated proteins Cytc and Bax were increased in HK-2 cells cultured in high glucose, all of which promoted the caspase cascade reaction, leading to increased caspase-9 and caspase-3 shear fragments inducing apoptosis of the mitochondrial pathway. Inhibition of MIR503HG led to a reduction in miR-503 expression, up-regulated its target gene Bcl-2, inhibited the expression levels of Bax and other apoptosis-related proteins and attenuated HK-2 cell apoptosis induced by high glucose. Co-transfection of miRNA-503 partially offset the effect of MIR503HG-siRNA. Conclusion: MIR503HG indirectly regulates Bcl-2 by promoting the co-transcription of miRNA-503 to participate high-glucose-induced proximal tubular cell apoptosis, providing a new target for diabetic nephropathy treatment.

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“…Microvascular endothelial cell (MVEC) is a barrier between blood and tissue, and regulates and stabilizes the blood and tissue environment by secreting a variety of bioactive substances. At the same time, studies also show that MVEC is an important target cell of many toxins, viruses and other pathogenic factors [14]. At present, the antioxidant activity of onion and garlic is rarely studied by endothelial cells.…”

Section: Introductionmentioning

confidence: 99%

In vitro Evaluation of Antibacterial Activity and Protective Effects on Cardiomyocytes with H/R Injury of Garlic/Onion Oil

Lü¹,

Lv²,

Li³

et al. 2020

Preprint

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Background: At present, the research concerning in vitro experiments of garlic oil and onion oil is limited. The objective of this study was to carry out the research on the effective components of garlic and onion, and to study the antibacterial activity of the two essential oils and their protective effects on cardiomyocytes with hypoxia/reoxygenation (H/R) injury.Method: The protective effect of volatile oils at different concentrations (200, 100, 50, 25, 12.5, 6.3, 3.1mg/L) on the endothelial cell of microvascular in cardiac muscle against H/R injury was examined by MTT and flow cytometer method. The survival rate and apoptosis situation were record. Inhibition zone test was used to evaluate antibacterial activity of volatile oils. MIC and MBC were calculated as well.Results: To achieve a higher survival rate, the optimum concentrations of garlic oil and onion oil were 12.5mg/L and 6.13mg/L and high concentrations of garlic and onion oil decreased the survival rate. Both the 12.5mg/L onion and garlic oil reduced the apoptosis situation of cardiomyocytes. Both garlic oil and onion oil had antibacterial effect on gram-positive bacteria and gram-negative bacteria, and had the best antibacterial effect on cocci of gram-positive bacteria.Conclusion: Garlic and onion oil do have antibacterial activity and protective effects on cardiomyocytes with H/R injury in a concentration range.

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miR-503/Apelin-12 mediates high glucose-induced microvascular endothelial cells injury via JNK and p38MAPK signaling pathway

Cited by 19 publications

References 40 publications

The Causes and Consequences of miR-503 Dysregulation and Its Impact on Cardiovascular Disease and Cancer

The Causes and Consequences of miR-503 Dysregulation and Its Impact on Cardiovascular Disease and Cancer

<p>LncRNA MIR503HG Promotes High-Glucose-Induced Proximal Tubular Cell Apoptosis by Targeting miR-503-5p/Bcl-2 Pathway</p>

In vitro Evaluation of Antibacterial Activity and Protective Effects on Cardiomyocytes with H/R Injury of Garlic/Onion Oil

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