The Effects and Mechanism of miR-92a and miR-126 on Myocardial Apoptosis in Mouse Ischemia-Reperfusion Model

Jiang, Changhao; Ji, Ningfei; Luo, Guopei; Ni, Shimao; Zong, Jinbo; Chen, Zhili; Bao, Dandan; Gong, Xinyan; Fu, Ting

doi:10.1007/s12013-014-0149-4

Cited by 20 publications

(20 citation statements)

References 29 publications

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“…Jiang and colleagues (Jiang et al, 2014), however, suggested recently that miR-126 may participate in myocardial cell apoptosis via heat shock protein 70. The target genes of miR-126 were not confirmed in this study and require further investigation to allow for the exact mechanism of miR-126 in the regulation of myocardial cell apoptosis to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

Effect and mechanism of miR-126 in myocardial ischemia reperfusion

Huang

2015

Genet. Mol. Res.

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ABSTRACT.Multiple studies have shown microRNAs to play an important role in disease occurrence and development. The role of miRNAs in ischemia-reperfusion injury, however, requires further investigation and the aim of this study was therefore to assess miR-126 expression in myocardial ischemia reperfusion and the effects of miR-126 on myocardial ischemia-reperfusion injury. An in vitro model of ischemia-reperfusion injury was established using rat myocardial H9c2 cells and miR-126 expression in these cells was assessed by real-time PCR. The miR-126 mimic and inhibitor were transfected into H9c2 cells before the injury was induced. Flow cytometry and western blotting were used to assess myocardial cell apoptosis. The triphenyltetrazolium chloride method was used to assess the infarction area and a TUNEL assay was used to analyze myocardial cell apoptosis. The results of the western blot analyses indicate that the miR-126 mimic and inhibitor increase and decrease caspase 3 degradation in myocardial cells, respectively. The in vivo experiments, moreover, revealed that the miR-126 mimic and inhibitor increase and reduce the myocardial infarction area, respectively. The TUNEL assay results showed increases and decreases in apoptotic myocardial cell numbers after infusion with the miR-126 mimic or inhibitor, respectively. These findings indicate that miRmiR-126 in myocardial ischemia reperfusion 18991©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 18990-18998 (2015) 126 is down-regulated in myocardial ischemia-reperfusion injury and that the inhibition of miR-126 may protect against myocardial cell apoptosis caused by ischemia-reperfusion.

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Section: Discussionmentioning

confidence: 99%

Effect and mechanism of miR-126 in myocardial ischemia reperfusion

Huang

2015

Genet. Mol. Res.

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“…Inflammation‐related targets of miR‐146a include IL‐1 receptor‐associated kinase‐1 (IRAK1), TNF receptor‐associated factor 6 (TRAF6), and IL‐1β. MiR‐126 regulates the expression of vascular adhesion molecules and is implicated in ER stress expression as it can modulate the heat stress protein Hsp70 …”

Section: Introductionmentioning

confidence: 99%

“…MiR-126 regulates the expression of vascular adhesion molecules and is implicated in ER stress expression as it can modulate the heat stress protein Hsp70. 18 In this study, we investigated the effects of maternally administered melatonin on LPS-induced brain cellular stress. We report here that maternal lipopolysaccharide (LPS) sensitizes the immature rat brain to a second postnatal excitotoxic injury.…”

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confidence: 99%

Melatonin modulates neonatal brain inflammation through endoplasmic reticulum stress, autophagy, and miR‐34a/silent information regulator 1 pathway

Carloni

Favrais

Saliba

et al. 2016

Journal of Pineal Research

115

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Maternal infection/inflammation represents one of the most important factors involved in the etiology of brain injury in newborns. We investigated the modulating effect of prenatal melatonin on the neonatal brain inflammation process resulting from maternal intraperitoneal (i.p.) lipopolysaccharide (LPS) injections. LPS (300 μg/kg) was administered to pregnant rats at gestational days 19 and 20. Melatonin (5 mg/kg) was administered i.p. at the same time as LPS. Melatonin counteracted the LPS sensitization to a second ibotenate-induced excitotoxic insult performed on postnatal day (PND) 4. As melatonin succeeded in reducing microglial activation in neonatal brain at PND1, pathways previously implicated in brain inflammation regulation, such as endoplasmic reticulum (ER) stress, autophagy and silent information regulator 1 (SIRT1), a melatonin target, were assessed at the same time-point in our experimental groups. Results showed that maternal LPS administrations resulted in an increase in CHOP and Hsp70 protein expression and eIF2α phosphorylation, indicative of activation of the unfolded protein response consequent to ER stress, and a slighter decrease in the autophagy process, determined by reduced lipidated LC3 and increased p62 expression. LPS-induced inflammation also reduced brain SIRT1 expression and affected the expression of miR-34a, miR146a, and miR-126. All these effects were blocked by melatonin. Cleaved-caspase-3 apoptosis pathway did not seem to be implicated in the noxious effect of LPS on the PND1 brain. We conclude that melatonin is effective in reducing maternal LPS-induced neonatal inflammation and related brain injury. Its role as a prophylactic/therapeutic drug deserves to be investigated by clinical studies.

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“…Our previous studies showed that long-term intermittent hypoxia could result in eccentric cardiac hypertrophy in rats (Chen et al, 2007) and induce both mitochondrial-dependent apoptotic and Fas death receptor-dependent apoptotic pathways in rat hearts (Lee et al, 2007). Results from several studies suggested that cardiomyocyte apoptosis is a critical factor in the initiation and progression of many types of cardiac disease (Konstantinidis et al, 2012) such as ischemia/reperfused heart MI and end-stage heart failure (Jiang et al, 2014;Lim et al, 2014;Xu et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Long-term hypoxia exposure enhanced IGFBP-3 protein synthesis and secretion resulting in cell apoptosis in H9c2 myocardial cells

et al. 2015

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Myocardial infarction (MI) usually results in myocardial ischemia, remodeling and hypoxia that lead to cell death. To date, the insulin-like growth factor binding protein-3 (IGFBP3) is known to play an important role in insulin growth factor (IGF) bioavailability. Previous studies have found that hypoxia results in cell apoptosis. However, the detailed mechanism and roles of IGFBP3 in long-term hypoxia (LTH) regulated heart cell apoptosis remains unknown. In this study H9c2 cardiomyoblast cells were treated with investigated long-term hypoxic exposure with the possible mechanisms involved. The results showed that LTH enhanced IGFBP3 protein synthesis and induced its secretion. The accumulated IGFBP3 sequestered Insulin growth factor 1 (IGF-1) away from the type I IGF receptor (IGF-1 R), which blocked the IGF1R/PI3K/Akt survival signaling pathway, resulting in cell apoptosis. According to our findings, IGFBP3 could be a valuable target for developing treatments for cardiac diseases in long-term hypoxia exposure patients.

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The Effects and Mechanism of miR-92a and miR-126 on Myocardial Apoptosis in Mouse Ischemia-Reperfusion Model

Cited by 20 publications

References 29 publications

Effect and mechanism of miR-126 in myocardial ischemia reperfusion

Effect and mechanism of miR-126 in myocardial ischemia reperfusion

Melatonin modulates neonatal brain inflammation through endoplasmic reticulum stress, autophagy, and miR‐34a/silent information regulator 1 pathway

Long-term hypoxia exposure enhanced IGFBP-3 protein synthesis and secretion resulting in cell apoptosis in H9c2 myocardial cells

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