Cross Talk Between the Notch Signaling and Noncoding RNA on the Fate of Stem Cells

Tang, Yaoliang; Wang, Yingjie; Chen, Lijuan; Pan, Yaohua; Weintraub, Neal L.

doi:10.1016/b978-0-12-398459-3.00008-3

Cited by 12 publications

(11 citation statements)

References 107 publications

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“…Mature miRNAs can mediate translational repression by forming miRNA-induced silencing complexes, which bind to the 3′-untranslated region (3′UTR) of target mRNAs [8]. MiRNAs have been reported previously to play important roles in regulating cell apoptosis [9–11] and the progression of vascular diseases [12, 13].…”

Section: Introductionmentioning

confidence: 99%

miR-92a inhibits vascular smooth muscle cell apoptosis: role of the MKK4–JNK pathway

et al. 2014

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Vascular smooth muscle cell (VSMC) apoptosis plays an important role in vascular remodeling and atherosclerotic plaque instability. Oxidative stress in diseased vessels promotes VSMC apoptosis in part by activating the c-Jun N-terminal kinase (JNK) pathway, which has been identified as a molecular target of miR-92a in macrophages. Here, we examined the expression and biological activity of miR-92a in VSMC. Quiescent VSMC exhibited a low basal expression of miR-92a, which was positively regulated by serum stimulation and negatively regulated by H2O2. Overexpression of miR-92a decreased H2O2-induced VSMC apoptosis as indicated by TUNEL assay and cleaved caspase-3 protein levels. Using 3′UTRreporter assay, we found that miR-92a overexpression led to suppression of both mitogen-activated protein kinase kinase 4 (MKK4)- and JNK1-dependent luciferase activity. We also found that 10 mer seed match between miRNA: mRNA pair is more efficient than 8 mer seed match for us to identify authentic miRNA target. Protein levels of active phospho-JNK and phospho-c-Jun, downstream targets of the MKK4–JNK1 pathway, were also decreased by overexpressing miR-92a in VSMC under oxidative stress. Consistent with these findings, overexpression of MKK4 reversed the anti-apoptotic effects of miR-92a in oxidatively stressed VSMC. In conclusion, miR-92a overexpression inhibits H2O2-induced VSMC apoptosis by directly targeting the MKK4–JNK1 pathway.

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Section: Introductionmentioning

confidence: 99%

miR-92a inhibits vascular smooth muscle cell apoptosis: role of the MKK4–JNK pathway

et al. 2014

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“…Mature miRNAs can form miRNA-induced silencing complexes, which bind to the 3′-untranslated region (3′UTR) of target mRNAs to mediate translational repression [6]. Previous studies have suggested that miRNAs play important roles in regulating cell apoptosis [7–9] and the progression of vascular disease [10, 11].…”

Section: Introductionmentioning

confidence: 99%

MiR-92a regulates viability and angiogenesis of endothelial cells under oxidative stress

Zhang

Zhou

Qin

et al. 2014

Biochemical and Biophysical Research Communications

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Oxidative stress contributes to endothelial cell (EC) dysfunction, which is prevalent in ageing and atherosclerosis. MicroRNAs (miRs) are small, non-coding RNAs that post-transcriptionally regulate gene expression and play a key role in fine-tuning EC functional responses, including apoptosis and angiogenesis. MiR-92a is highly expressed in young endothelial cells in comparison with senescent endothelial cells, which exhibit increased oxidative stress and apoptosis. However, the impact of miR-92a treatment on EC viability and angiogenesis under oxidative stress is unknown. Hydrogen peroxide (H2O2) was used to induce oxidative stress in human umbilical vein endothelial cells (HUVEC). Pre-miR-92a treatment decreased H2O2–induced apoptosis of HUVEC as determined by TUNEL assay. Pre-miR-92a treatment enhanced capillary tube formation by HUVEC under oxidative stress, which was blocked by LY294002, an inhibitor of Akt phosphorylation. Interestingly, we also observed that inhibition of miR-92a by anti-miR-92a antisense can also enhance angiogenesis in HUVEC with and without oxidative stress exposure. Our results show that perturbation of miR-92a levels outside of its narrow “homeostatic” range may trigger endothelial cell angiogenesis, suggesting that the role of miR-92a in regulating angiogenesis is controversial and may vary depending on the experimental model and method of regulating miR-92a.

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“…Notch activity may be affected by microRNAs [437]. Various microRNAs negatively regulate Fbw7 expression including miR-27a, miR-182, miR-363~92, and miR-223 [253, 438, 439] and may increase the expression of Fbw7-regulated target genes including Notch1, Mcl-1, c-Jun, c-Myc, and Cyclin E [438].…”

Section: Parameters Affecting the Susceptibility Of Lymphoid Maligmentioning

confidence: 99%

MicroRNAs and Glucocorticoid-Induced Apoptosis in Lymphoid Malignancies

Sionov

2013

ISRN Hematology

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The initial response of lymphoid malignancies to glucocorticoids (GCs) is a critical parameter predicting successful treatment. Although being known as a strong inducer of apoptosis in lymphoid cells for almost a century, the signaling pathways regulating the susceptibility of the cells to GCs are only partly revealed. There is still a need to develop clinical tests that can predict the outcome of GC therapy. In this paper, I discuss important parameters modulating the pro-apoptotic effects of GCs, with a specific emphasis on the microRNA world comprised of small players with big impacts. The journey through the multifaceted complexity of GC-induced apoptosis brings forth explanations for the differential treatment response and raises potential strategies for overcoming drug resistance.

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Cross Talk Between the Notch Signaling and Noncoding RNA on the Fate of Stem Cells

Cited by 12 publications

References 107 publications

miR-92a inhibits vascular smooth muscle cell apoptosis: role of the MKK4–JNK pathway

miR-92a inhibits vascular smooth muscle cell apoptosis: role of the MKK4–JNK pathway

MiR-92a regulates viability and angiogenesis of endothelial cells under oxidative stress

MicroRNAs and Glucocorticoid-Induced Apoptosis in Lymphoid Malignancies

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