Overexpression of microRNA-378 attenuates ischemia-induced apoptosis by inhibiting caspase-3 expression in cardiac myocytes

Ji, Fang; Song, Xiaowei; Tian, Jing; Chen, Huyan; Li, Dongfeng; Wang, Jianfei; Ren, An‐Jing; Wang, Yuan; Lin, Li

doi:10.1007/s10495-011-0683-0

Cited by 136 publications

(98 citation statements)

References 38 publications

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“…miR-15 and miR-16 were found to induce apoptosis in chronic lymphocytic leukemia cells by regulating bcl-2 expression (Cimmino et al, 2005). Fang et al showed that miR-378 can inhibit the expression of its target gene caspase-3, thereby reducing ischemic injury in myocardial cells (Fang et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Keloid microRNA expression analysis and the influence of miR-199a-5p on the proliferation of keloid fibroblasts

Liang

et al. 2014

Genet. Mol. Res.

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ABSTRACT. The purpose of this study was to identify microRNAs (miRNAs) involved in keloid formation and determine their influence on the proliferation of keloid fibroblasts (KFs). Eight specimens each of resected keloid tissue and normal skin tissue were collected. miRNAs that are differentially expressed in keloid tissue and normal skin were detected using an miRNA microarray and verified by quantitative realtime polymerase chain reaction (RT-PCR). Seventeen differentially expressed miRNAs, including miR-199a-5p, were identified by microarray hybridization. qRT-PCR analysis confirmed the decrease in miR-199a-5p expression in keloid vs normal tissue that was detected by the microarray analysis. Mimics of differentially expressed miRNAs were then transfected into a KF cell line, and the effect of miRNA overexpression on the proliferation of KFs was assayed using the EdU assay. Compared with mock-transfected cells, KFs transfected with a miR-199a-5p mimic showed significantly lower cell proliferation and an altered cell cycle, with cells having significantly longer S and G2/M phases. The significantly lower expression of miRNA-199a-5p in keloids likely influences the cell cycle of KFs and restrains their proliferation, suggesting that miR-199a-5p probably plays a role in the regulation of KF proliferation.

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Section: Discussionmentioning

confidence: 99%

Keloid microRNA expression analysis and the influence of miR-199a-5p on the proliferation of keloid fibroblasts

Liang

et al. 2014

Genet. Mol. Res.

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“…The cells were routinely cultured in Dulbecco's modified Eagle's medium (DMEM) as previously described with minor modifications (Fang et al, 2012). The medium was changed every 2 d and when confluence was reached, the cells were subcultured by detaching with 0.25% trypsin-EDTA solution and re-seeding into new plates at a ratio of 1:5.…”

Section: Cell Culturementioning

confidence: 99%

Cardioprotective effects of fucoidan against hypoxia-induced apoptosis in H9c2 cardiomyoblast cells

Zhang

Xie

et al. 2015

Pharmaceutical Biology

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Context: Cardiomyocyte apoptosis plays a critical role in the progress of heart diseases. Fucoidan, a complex-sulfated polysaccharide, has been reported to possess potential cardioprotective efficacy in vivo. Objective: The present study determines whether fucoidan could provide cardioprotection on hypoxia-induced cardiomyocyte apoptosis. Materials and methods: H9c2 cardiomyoblast cells were incubated with various concentrations (15, 30, and 60 lg/ml) of fucoidan in a humidified incubator at 37 C with 95% O 2 and 5% CO 2 . After 6 h, hypoxia was processed and the cardioprotective effects of fucoidan were evaluated by applying MTT, ELISA, Hoechst 33258 nucleus staining, and western blot.Results: Following a 6 h exposure of H9c2 to hypoxic condition, significant reduction was found in cell survival (0.57-fold) and superoxide dismutase (SOD) activity (0.56-fold), which were associated with the increase of malondialdehyde (MDA) level (2.58-fold), creatine phosphokinase (CK, 3.57-fold), and lactate dehydrogenase (LDH) activities (2.39-fold). Moreover, hypoxiainduced apoptosis was confirmed by Hoechst 33258 nuclear staining, and these changes were accompanied by the increase of Bcl-2 (1.27-fold) and Bax expression (2.6-fold). However, preincubation of the cells with fucoidan prior to hypoxia exposure elevated the cell viability (30 lg/ml, 1.18-fold; 60 lg/ml, 1.32-fold) and SOD activity (30 lg/ml, 1.12-fold; 60 lg/ml, 1.25-fold), but decreased the MDA level (30 lg/ml, 0.70-fold; 60 lg/ml, 0.80-fold), CK (30 lg/ml, 0.69-fold; 60 lg/ml, 0.76-fold), and LDH (30 lg/ml, 0.67-fold; 60 lg/ml, 0.86-fold) leakages. Hoechst 33258 nuclear staining observations demonstrated the same protective effect of fucoidan on hypoxia-induced myocardial injury. Also, cardioprotective effects of fucoidan were reflected by increasing Bcl-2 (60 lg/ml, 1.84-fold), as well as decreasing Bax (60 lg/ml, 0.6-fold). Conclusion: Fucoidan had protective effect against hypoxia-induced cardiomyocytes apoptosis, and the mechanism might involve protections of the cell from oxidative injury.

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“…There is an extensive and growing list of miRNAs regulated by hypoxia, either positively or negatively, in different experimental settings (Kulshreshtha et al, 2008;Loscalzo, 2010;Bussolati et al, 2012;Du et al, 2012;Fang et al, 2012;Guo et al, 2012;Voellenkle et al, 2012). Other miRNAs are hypoxia-independent, but are capable of negatively regulating HIF; these include miR-107, miR-17-92 and miR-519c, whose expression is induced by p53, c-myc and the hepatocyte growth factor (HGF), respectively (Taguchi et al, 2008;Cha et al, 2010;Yamakuchi et al, 2010).…”

Section: Mirnas Participate In Negative and Positive Feedback Loops Tmentioning

confidence: 99%

Robustness of the hypoxic response: Another job for miRNAs?

Ezcurra

Bertolin

Melani

et al. 2012

Developmental Dynamics

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Living organisms are constantly exposed to environmental and genetic perturbations. Biological robustness enables these organisms to maintain their functional stability in the presence of external or internal changes. It has been proposed that microRNAs (miRNAs), small non-coding regulatory RNAs, contribute to robustness of gene regulatory networks. The hypoxic response is a major and well-characterized example of a cellular and systemic response to environmental stress that needs to be robust. miRNAs regulate the response to hypoxia, both at the level of the main transcription factor that mediates this response, the hypoxia-inducible factor (HIF), and at the level of one of the most important systemic outcomes of the response: angiogenesis. In this review, we will take the hypoxic response as a paradigm of miRNAs participating in circuits that provide robustness to biological responses.

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Overexpression of microRNA-378 attenuates ischemia-induced apoptosis by inhibiting caspase-3 expression in cardiac myocytes

Cited by 136 publications

References 38 publications

Keloid microRNA expression analysis and the influence of miR-199a-5p on the proliferation of keloid fibroblasts

Keloid microRNA expression analysis and the influence of miR-199a-5p on the proliferation of keloid fibroblasts

Cardioprotective effects of fucoidan against hypoxia-induced apoptosis in H9c2 cardiomyoblast cells

Robustness of the hypoxic response: Another job for miRNAs?

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