Protective effect of microRNA-30b on hypoxia/reoxygenation-induced apoptosis in H9C2 cardiomyocytes

Li, Tong; Sun, Zelin; Xie, Qi

doi:10.1016/j.gene.2015.02.051

Cited by 13 publications

(14 citation statements)

References 42 publications

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“…The mechanisms involved in miRNA‐mediated protection against I/R injury appear to be related to the decreased apoptosis of myocardial cells [Qin et al, ]. Interestingly, miR‐30b‐mediated protection against I/R induced apoptosis implicates in targeting KRAS gene and augmenting Ras–PI3K–Akt activation, thus, over‐expression of miR‐30b can inhibit I/R induced cardiomyocyte apoptosis [Leite‐Moreira et al, ; Liao et al, ; Li et al, ]. Our study investigated if the anti‐apoptotic effects of miR‐30b extended to the cardiovascular system and more importantly, if these functions had relevance to I/R injury, and therefore, we tested this hypothesis using the early phase of rat I/R injury model.…”

mentioning

confidence: 99%

Retracted: Anti‐Apoptotic Effect of MicroRNA‐30b in Early Phase of Rat Myocardial Ischemia‐Reperfusion Injury Model

Song

Liu

Wang

et al. 2015

J of Cellular Biochemistry

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This study aimed to investigate the effect of microRNA-30b (miR-30b) in rat myocardial ischemic-reperfusion (I/R) injury model. We randomly divided Sprague-Dawley (SD) rats (n = 80) into five groups: 1) control group; 2) miR-30b group; 3) sham-operated group; 4) I/R group, and 5) I/R+miR-30b group. Real-time quantitative polymerase chain reaction, immunohistochemical staining and Western blot analysis were conducted. TUNEL assay was employed for testing cardiomyocyte apoptosis. Our results showed that miR-30b levels were down-regulated in I/R group and I/R + miR-30b group compared with sham-operated group (both P < 0.05). However, miR-30b level in I/R + miR-30b group was higher than I/R group (P < 0.05). Markedly, the apoptotic rate in I/R group showed highest in I/R group (P < 0.05). Additionally, the results illustrated that protein levels of Bcl-2, Bax, and caspase-3 were at higher levels in ischemic regions in I/R group, comparing to sham-operated group (all P < 0.05), while Bcl-2/Bax was reduced (P < 0.05). Bcl-2 level and Bcl-2/Bax were obviously increased in I/R + miR-30b group by comparison with I/R group, and expression levels of Bax and caspase-3 were down-regulated (all P < 0.05). We also found that in I/R + miR-30b group, KRAS level was apparently lower and p-AKT level was higher by comparing with I/R group (both P < 0.05). Our study indicated that miR-30b overexpression had anti-apoptotic effect on early phase of rat myocardial ischemia injury model through targeting KRAS and activating the Ras/Akt pathway.

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confidence: 99%

Retracted: Anti‐Apoptotic Effect of MicroRNA‐30b in Early Phase of Rat Myocardial Ischemia‐Reperfusion Injury Model

Song

Liu

Wang

et al. 2015

J of Cellular Biochemistry

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“…Previous studies have shown that miR-30b is involved in cell apoptosis by regulating the expression of caspase-3. Li constructed the ischemia-reperfusion (I/R) injury model in H2C9 rat myocardial cells and found the overexpression of miR-30b down-regulated the expression of caspase-3 and improve I/R injury in H2C9 cells [ 29 ]. Similarly, Song et al , demonstrated that miR-30b levels were down-regulated by I/R injury in rat myocardial cells.…”

Section: Discussionmentioning

confidence: 99%

MiR-30b Is Involved in the Homocysteine-Induced Apoptosis in Human Coronary Artery Endothelial Cells by Regulating the Expression of Caspase 3

Chen

Song

et al. 2015

IJMS

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Homocysteine (Hcy) is an independent risk factor for a variety of cardiovascular diseases, such as coronary heart disease, hypertension, stroke, etc. There is a close relationship between the vascular endothelial cell apoptosis and these diseases. Recent studies have shown homocysteine can induce apoptosis in endothelial cells, which may be an important mechanism for the development of theses cardiovascular diseases. Although there are several reports about how the Hcy induces apoptosis in endothelial cells, the exact mechanism is not fully understood. MicroRNAs are small, non-coding RNA. Previous studies have shown that there is a close relationship between several microRNAs and cell apoptosis. However, there are no studies about the role of microRNAs in Hcy-induced apoptosis in endothelial cells so far. In this study, we constructed the model of homocysteine-induced apoptosis in human coronary artery endothelial cells (HCAECs) and found miR-30b was significantly down-regulated by 1 mmol/L Hcy. In addition, overexpression of miR-30b can improve the Hcy-induced apoptosis in HCAECs by downregulating caspase-3 expression. Therefore, miR-30b may play an important role in Hcy-induced apoptosis in endothelial cells.

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“…Particularly, treatment with high Pi levels significantly downregulated miR-30b expression. A previous study showed that miR-30b overexpression improved ischemia-reperfusion (I/R) injury in H2C9 cells by downregulating caspase-3 [23]. Similarly, Song et al found that I/R injury decreased miR-30b expression in rat myocardial cells [24].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-30b Regulates High Phosphorus Level-Induced Autophagy in Vascular Smooth Muscle Cells by Targeting BECN1

Wang

Sun

et al. 2017

Cell Physiol Biochem

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Background/Aims: Autophagy is an evolutionarily conserved mechanism that affects the survival and functions of vascular smooth muscle cells (VSMCs). We explored the role of microRNAs (miRNAs) in regulating autophagy in VSMCs exposed to high phosphorus (Pi) levels. Methods: VSMCs were isolated from the thoracic aorta of rats and were cultured primarily. Real-time PCR was used to measure the mRNA expression of indicated genes. Western blotting was performed to detect the protein expression of autophagy-related markers. Results: We found that treatment with high Pi levels (1 and 3 mM) activated LC3II expression and promoted autophagic flux in VSMCs. Conversely, treatment with an autophagy inhibitor decreased LC3II expression. Pi stimulation dysregulated the expression of several miRNAs such as miR-18a, miR-21, miR-23a, miR-30b, and miR-31a. However, miR-30b overexpression decreased Pi-induced expression of autophagy-related marker genes such as BECN1, ATG5, and LC3b, whereas miR-30b downregulation increased Pi-induced expression of these genes. In addition, we found that miR-30b directly targeted BECN1. Conclusions: These data suggest that miR-30b plays an important role in the regulation of high Pi level-induced autophagy in VSMCs by targeting BECN1.

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Protective effect of microRNA-30b on hypoxia/reoxygenation-induced apoptosis in H9C2 cardiomyocytes

Cited by 13 publications

References 42 publications

Retracted: Anti‐Apoptotic Effect of MicroRNA‐30b in Early Phase of Rat Myocardial Ischemia‐Reperfusion Injury Model

Retracted: Anti‐Apoptotic Effect of MicroRNA‐30b in Early Phase of Rat Myocardial Ischemia‐Reperfusion Injury Model

MiR-30b Is Involved in the Homocysteine-Induced Apoptosis in Human Coronary Artery Endothelial Cells by Regulating the Expression of Caspase 3

MicroRNA-30b Regulates High Phosphorus Level-Induced Autophagy in Vascular Smooth Muscle Cells by Targeting BECN1

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