Absence of miR-223-3p ameliorates hypoxia-induced injury through repressing cardiomyocyte apoptosis and oxidative stress by targeting KLF15

Tang, Qing; Li, Mingyue; Su, Yufei; Fu, Jia; Zou, Zongyi; Wang, Yi; Li, Shaoning

doi:10.1016/j.ejphar.2018.10.014

Cited by 36 publications

(28 citation statements)

References 23 publications

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“…miR-223 has a negative role in hypoxia-induced cardiomyocyte apoptosis, in which silence of miR-223 improved hypoxia-induced H9C2 cell injury through preventing apoptosis accompanied by an increase of Bcl-2 expression and a decrease of Bax and cleaved caspase-3 expression. 10,17 In this study, inhibition of miR-223 expression distinctly reduced H 2 O 2induced cardiomyocyte apoptosis, increased expression of the anti-apoptotic protein Bcl-2, and reduced expression of the pro-apoptotic proteins Bax and cleaved caspase-3. Our data revealed that miR-233 played a negative role in H 2 O 2 -induced cardiomyocyte apoptosis.…”

Section: Discussionsupporting

confidence: 48%

Silencing of miR-223 expression inhibits the apoptosis of H₂O₂-induced cardiomyocytes by increasing the activity of the IGF-1R/PI3K/AKT pathway

Zhou

2020

Eur J Inflamm

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To study the: (1) function of micro (mi)R-223 on H2O2-induced H9C2 cells; (2) relationship between miR-223 and insulin-like growth factor 1 receptor (IGF-1R); and (3) role of miR-223 on the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway. H9C2 cells were selected to establish the H2O2-injury model. Overexpression/low expression of miR-223 in H9C2 cells was constructed, respectively. Flow cytometry and western blotting were applied to measure the apoptosis, cell activity, and expression of related proteins. Dual-luciferase reporter gene assays (DLRGAs) were applied to test if miR-223 targeted IGF-1R. Overexpression/low expression of IGF-1R was constructed to test if miR-223 regulated IGF-1R expression negatively. Increases in miR-223 expression were observed in H2O2-induced H9C2 cells. miR-223 absence improved H2O2-induced H9C2-cell apoptosis accompanied by an increase in B-cell lymphoma (Bcl)-2 expression and decrease in expression of Bax and cleaved caspase-3 ( P < 0.05). miR-223 silencing increased expression of IGF-1R, p-PI3K, and p-AKT in H2O2-induced H9C2 cells ( P < 0.05). miR-223 overexpression aggravated H2O2-induced H9C2-cell apoptosis and reduced expression of the proteins of IGF-1R, p-PI3K, and p-AKT. DLRGAs showed IGF-1R to be a downstream gene of miR-223. IGF-1R silencing significantly inhibited expression of p-PI3K and p-AKT proteins ( P < 0.05). miR-223 negatively regulated IGF-1R expression for H9C2-cell apoptosis and the PI3K/AKT pathway. miR-223 absence can ameliorate H2O2-induced cardiomyocyte apoptosis by targeting IGF-1R to regulate PI3K/AKT activity.

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Section: Discussionsupporting

confidence: 48%

Silencing of miR-223 expression inhibits the apoptosis of H₂O₂-induced cardiomyocytes by increasing the activity of the IGF-1R/PI3K/AKT pathway

Zhou

2020

Eur J Inflamm

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“…Lastly, miR-223-3p levels are increased in hypoxic cardiomyocytes and inhibition of miR-223-3p was able to prevent hypoxia-induced apoptosis and delay oxidative stress by inhibiting ROS generation and lipid peroxidation by targeting Kruppel like factor 15 (KLF15). Thus, decreased miR-223-3p levels also enhanced the expression of antioxidant enzymes, such as SOD, CAT, and GPx [96].…”

Section: Mirna and Ros Crosstalk During MImentioning

confidence: 94%

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Climent

Viggiani

Lin

et al. 2020

IJMS

101

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Reactive oxygen species (ROS) affect many cellular functions and the proper redox balance between ROS and antioxidants contributes substantially to the physiological welfare of the cell. During pathological conditions, an altered redox equilibrium leads to increased production of ROS that in turn may cause oxidative damage. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level contributing to all major cellular processes, including oxidative stress and cell death. Several miRNAs are expressed in response to ROS to mediate oxidative stress. Conversely, oxidative stress may lead to the upregulation of miRNAs that control mechanisms to buffer the damage induced by ROS. This review focuses on the complex crosstalk between miRNAs and ROS in diseases of the cardiac (i.e., cardiac hypertrophy, heart failure, myocardial infarction, ischemia/reperfusion injury, diabetic cardiomyopathy) and pulmonary (i.e., idiopathic pulmonary fibrosis, acute lung injury/acute respiratory distress syndrome, asthma, chronic obstructive pulmonary disease, lung cancer) compartments. Of note, miR-34a, miR-144, miR-421, miR-129, miR-181c, miR-16, miR-31, miR-155, miR-21, and miR-1/206 were found to play a role during oxidative stress in both heart and lung pathologies. This review comprehensively summarizes current knowledge in the field.

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“…With regards to previous studies, miR-223-3p is known to be involved in myocardial injury and positively correlates with cardiac apoptosis and oxidative stress through interaction with krüppel-like factor 15 (KLF-15). Furthermore, an inverse correlation of miR-223-3p with an improved cell viability, prevention of cardiomyocyte apoptosis as well as with inhibition of reactive oxygen species and lipid peroxidation was shown in a former study 26 . Similar, elevated levels of miR-223-3p were reported under simulated microgravity in rats with an inhibitory effect on hepatocyte proliferation trough a cyclin dependent kinase 2/Cullin1 (CDK2/CUL1) signaling pathway 11 .…”

Section: Discussionmentioning

confidence: 76%

Next-generation sequencing analysis of circulating micro-RNA expression in response to parabolic flight as a spaceflight analogue

et al. 2020

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Understanding physiologic reactions to weightlessness is an indispensable requirement for safe human space missions. This study aims to analyse changes in the expression of circulating miRNAs following exposure to gravitational changes. Eight healthy volunteers (age: 24.5 years, male: 4, female: 4) were included. Each subject underwent 31 short-term phases of weightlessness and hypergravity induced by parabolic flight as a spaceflight analogue. At baseline, 1 and 24 h after parabolic flight, venous blood was withdrawn. Analysis of circulating miRNAs in serum was conducted by means of next generation sequencing. In total, 213 miRNAs were robustly detected (TPM > 5) by small RNA sequencing in all 24 samples. Four miRNAs evidenced a significant change in expression after adjusting for multiple testing. Only miR-223-3p showed a consistent significant decrease 24 h after parabolic flight compared to baseline values and values at 1 h after parabolic flight. miR-941 and miR-24-3p showed a significant decrease 24 h after parabolic flight compared to 1 h after parabolic flight but not to baseline values. miR-486-5p showed a significant increase 24 h after parabolic flight compared to 1 h after parabolic flight but not to baseline values. A target network analysis identified genes of the p53 signaling pathway and the cell cycle highly enriched among the targets of the four microRNAs. Our findings suggest cellular adaption to gravitational changes at the post-transcriptional level. Based on our results, we suggest a change in cell cycle regulation as potential explanation for adaptational changes observed in space missions.

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Absence of miR-223-3p ameliorates hypoxia-induced injury through repressing cardiomyocyte apoptosis and oxidative stress by targeting KLF15

Cited by 36 publications

References 23 publications

Silencing of miR-223 expression inhibits the apoptosis of H₂O₂-induced cardiomyocytes by increasing the activity of the IGF-1R/PI3K/AKT pathway

Silencing of miR-223 expression inhibits the apoptosis of H₂O₂-induced cardiomyocytes by increasing the activity of the IGF-1R/PI3K/AKT pathway

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Next-generation sequencing analysis of circulating micro-RNA expression in response to parabolic flight as a spaceflight analogue

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Absence of miR-223-3p ameliorates hypoxia-induced injury through repressing cardiomyocyte apoptosis and oxidative stress by targeting KLF15

Cited by 36 publications

References 23 publications

Silencing of miR-223 expression inhibits the apoptosis of H2O2-induced cardiomyocytes by increasing the activity of the IGF-1R/PI3K/AKT pathway

Silencing of miR-223 expression inhibits the apoptosis of H2O2-induced cardiomyocytes by increasing the activity of the IGF-1R/PI3K/AKT pathway

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Next-generation sequencing analysis of circulating micro-RNA expression in response to parabolic flight as a spaceflight analogue

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Silencing of miR-223 expression inhibits the apoptosis of H₂O₂-induced cardiomyocytes by increasing the activity of the IGF-1R/PI3K/AKT pathway

Silencing of miR-223 expression inhibits the apoptosis of H₂O₂-induced cardiomyocytes by increasing the activity of the IGF-1R/PI3K/AKT pathway