Effects of down-regulation of microRNA-23a on TNF-α-induced endothelial cell apoptosis through caspase-dependent pathways

Ruan, Wei; Xu, Junmei; Li, Suo-bei; Yuan, Ling‐Qing; Dai, Rongping

doi:10.1093/cvr/cvr290

Cited by 63 publications

(46 citation statements)

References 45 publications

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“…5B to G). This set included reporters for CASP3 and CASP7, which had previously been shown to be repressed by miR-K3 and miR-23a, respectively (34,55).To verify that miR-K3 and miR-23a indeed exert their effect through the same PAR-CLIP-and/or TargetScan-predicted binding sites in these 3= UTRs, we introduced 2-nt mutations into each of the candidate seed matches. Results from these experiments confirmed that miR-K3 and miR-23a indeed regulate their targets through the same predicted sites (Fig.…”

Section: Resultsmentioning

confidence: 99%

Kaposi's Sarcoma-Associated Herpesvirus Encodes a Mimic of Cellular miR-23

Manzano

Shamulailatpam

Raja

et al. 2013

J Virol

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Kaposi's sarcoma-associated herpesvirus (KSHV) expresses ϳ20 viral microRNAs (miRNAs) in latently infected cells. We have previously shown that two of these miRNAs function as mimics of the cellular miRNAs miR-155 and miR-142-3p. Two additional KSHV miRNAs, miR-K3؉1 and miR-K3, share perfect and offset 5= homology with cellular miR-23, respectively. Here, we report a single nucleotide polymorphism that causes miR-K3؉1 expression in a subset of KSHV-infected primary effusion lymphoma cell lines as a consequence of altered processing of the primary transcript by the Microprocessor complex. We confirm that miR-K3؉1 regulates miR-23 targets, which is expected because these miRNAs share the entire seed region (nucleotides 2 to 8). Surprisingly, we found that miR-K3 also regulates miR-23 targets, despite offset seed sequences. In addition, the offset homology of miR-K3 to miR-23 likely allows this viral miRNA to expand its target repertoire beyond the targets of miR-23. Because miR-23 is highly expressed in endothelial cells but expressed at only low levels in B cells, we hypothesize that miR-K3 may function to introduce miR-23-like activities into KSHV-infected B cells. Together, our data demonstrate that KSHV has evolved at least three distinct viral miRNAs to tap into evolutionarily conserved cellular miRNA-regulatory networks. Furthermore, our data allow fundamental insights into the generation and functional impact of miRNA 5= end variation.

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Section: Resultsmentioning

confidence: 99%

Kaposi's Sarcoma-Associated Herpesvirus Encodes a Mimic of Cellular miR-23

Manzano

Shamulailatpam

Raja

et al. 2013

J Virol

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“…Real-time PCR assay protocol was performed using SYBR Green Real-Time PCR Master Mixes (Roche) as described by our previous studies (Ruan et al, 2012). PCR primers were 5 0 -GCCGACAGGATGCAGAAGG AGATCA-3 0 and 5 …”

Section: Rna Extraction Reverse Transcription and Real-time Pcrmentioning

confidence: 99%

Development of Anxiety-Like Behavior via Hippocampal IGF-2 Signaling in the Offspring of Parental Morphine Exposure: Effect of Enriched Environment

Luo

Cui

et al. 2014

Neuropsychopharmacol

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Opioid addiction is a major social, economic, and medical problem worldwide. Long-term adverse consequences of chronic opiate exposure not only involve the individuals themselves but also their offspring. Adolescent maternal morphine exposure results in behavior and morphologic changes in the brain of their adult offspring. However, few studies investigate the effect of adult opiate exposure on their offspring. Furthermore, the underlying molecular signals regulating the intergenerational effects of morphine exposure are still elusive. We report here that morphine exposure of adult male and female rats resulted in anxiety-like behavior and dendritic retraction in the dentate gyrus (DG) region of the hippocampus in their adult offspring. The behavior and morphologic changes were concomitant with the downregulation of insulin-like growth factor (IGF)-2 signaling in the granular zone of DG. Overexpression of hippocampal IGF-2 by bilateral intra-DG injection of lentivirus encoding the IGF-2 gene prevented anxiety-like behaviors in the offspring. Furthermore, exposure to an enriched environment during adolescence corrected the reduction of hippocampal IGF-2 expression, normalized anxietylike behavior and reversed dendritic retraction in the adult offspring. Thus, parental morphine exposure can lead to the downregulation of hippocampal IGF-2, which contributed to the anxiety and hippocampal dendritic retraction in their offspring. An adolescent-enriched environment experience prevented the behavior and morphologic changes in their offspring through hippocampal IGF-2 signaling. IGF-2 and an enriched environment may be a potential intervention to prevention of anxiety and brain atrophy in the offspring of parental opioid exposure.

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“…Additionally, tumor necrosis factor-α (TNF-α) is a contributing risk factor in atherosclerosis and common metabolic disturbances including insulin resistance and dyslipidemia (16). More specifically, TNF-α plays a key role as both an inflammatory mediator and inducer of apoptosis in endothelial cells (17,18). Evidence of these roles can be found in the increased plasma levels of TNF-α in diabetic patients, which have been shown to impair the function of endothelial cells, as well as to enhance their aging and apoptosis (19)(20)(21).…”

Section: Introductionmentioning

confidence: 99%

Simvastatin attenuates TNF-α-induced apoptosis in endothelial progenitor cells via the upregulation of SIRT1

Song

Zhang

et al. 2014

International Journal of Molecular Medicine

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Abstract. Endothelial progenitor cells (EPCs) originate from the bone marrow and can be classified as either early or late EPCs. The focus of this study was on late EPCs, as they play an important role in angiogenesis and vascular proliferation. Evidence suggests that inflammatory and oxidative changes can increase EPC apoptosis. Of note, tumor necrosis factor-α (TNF-α) is a contributing risk factor to the development of atherosclerosis and plays a key role as both an inflammatory mediator and an inducer of apoptosis in endothelial cells. Additionally, a member of the sirtuin family, silent information regulator type-1 (SIRT1), promotes cell survival by repressing p53-and non-p53-dependent apoptosis in response to DNA damage and oxidative stress. Statins have also been shown to play a key role in the prevention of endothelial apoptosis and senescence via their lipid-lowering and anti-inflammatory actions. However, there is little evidence that statins themselves attenuate EPC apoptosis induced by TNF-α. The aim of this study was to demonstrate the effectiveness of one of the most commonly used statins, simvastatin, on decreasing TNF-α-induced apoptosis in EPCs. The results indicated that SIRT1 protein expression was decreased by TNF-α in a time-and dose-dependent manner and that while TNF-α caused a marked increase in the percentage of apoptotic EPCs, application of simvastatin decreased this percentage. A high concentration of simvastatin promoted the expression of SIRT1 and increased the proliferation of EPCs. In conclusion, findings of this study showed that simvastatin is crucial in counteracting the TNF-α-induced apoptosis of EPCs and that this protection may involve the actions of SIRT1.

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Effects of down-regulation of microRNA-23a on TNF-α-induced endothelial cell apoptosis through caspase-dependent pathways

Abstract: Our results suggest that miR-23a may be involved in TNF-α-induced endothelial cell apoptosis through regulation of the caspase-7 and serine/threonine kinase 4-caspase-3 pathways.

Cited by 63 publications

References 45 publications

Kaposi's Sarcoma-Associated Herpesvirus Encodes a Mimic of Cellular miR-23

Kaposi's Sarcoma-Associated Herpesvirus Encodes a Mimic of Cellular miR-23

Development of Anxiety-Like Behavior via Hippocampal IGF-2 Signaling in the Offspring of Parental Morphine Exposure: Effect of Enriched Environment

Simvastatin attenuates TNF-α-induced apoptosis in endothelial progenitor cells via the upregulation of SIRT1

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