Pioglitazone up-regulates long non-coding RNA MEG3 to protect endothelial progenitor cells via increasing HDAC7 expression in metabolic syndrome

Liu, H.Z.; Wang, Q.Y.; Zhang, Y.; Qi, Datun; Li, M.W.; Guo, Weichun; Ma, Yuhui; Wang, L.Y.; Chen, Y.; Gao, Chunji

doi:10.1016/j.biopha.2016.01.001

Cited by 32 publications

(19 citation statements)

References 27 publications

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“…1). Another study also depicted a deleterious role of PA on EPCs in MetS patients via regulating lncRNA MEG3 [144]. MEG3 is required for human mesenchymal stem cells (hMSCs) differentiation into ECs [145]; however, some studies showed that MEG3 may also interfere with the proliferation and angiogenesis in VECs and its expression may correlate with cardiovascular aging [146].…”

Section: Role Of Ffas In Inducing Ed: Evidence From Clinical and Expementioning

confidence: 99%

Role of free fatty acids in endothelial dysfunction

et al. 2017

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Plasma free fatty acids levels are increased in subjects with obesity and type 2 diabetes, playing detrimental roles in the pathogenesis of atherosclerosis and cardiovascular diseases. Increasing evidence showing that dysfunction of the vascular endothelium, the inner lining of the blood vessels, is the key player in the pathogenesis of atherosclerosis. In this review, we aimed to summarize the roles and the underlying mechanisms using the evidence collected from clinical and experimental studies about free fatty acid-mediated endothelial dysfunction. Because of the multifaceted roles of plasma free fatty acids in mediating endothelial dysfunction, elevated free fatty acid level is now considered as an important link in the onset of endothelial dysfunction due to metabolic syndromes such as diabetes and obesity. Free fatty acid-mediated endothelial dysfunction involves several mechanisms including impaired insulin signaling and nitric oxide production, oxidative stress, inflammation and the activation of the renin-angiotensin system and apoptosis in the endothelial cells. Therefore, targeting the signaling pathways involved in free fatty acid-induced endothelial dysfunction could serve as a preventive approach to protect against the occurrence of endothelial dysfunction and the subsequent complications such as atherosclerosis.

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Section: Role Of Ffas In Inducing Ed: Evidence From Clinical and Expementioning

confidence: 99%

Role of free fatty acids in endothelial dysfunction

et al. 2017

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“…The authors found a mechanism by which MIR31HG enriched AcH3 and H3K4me3 in the promoter area of Fabp4 [ 112 ]. Moreover, the expression of lncRNA MEG3 was shown to be upregulated by pioglitazone to protect endothelial progenitor cells via decreasing miR-140-5p levels and increasing Hdac7 expression in subjects with metabolic syndrome [ 113 ]. MEG3 has also been shown to govern the balance between adipogenic and osteoblastogenic differentiation in human adipose-derived stem cells (hASCs) [ 114 ].…”

Section: Lncrnas In Metabolic Organsmentioning

confidence: 99%

Long Non-Coding RNAs in Metabolic Organs and Energy Homeostasis

Giroud

Scheideler

2017

IJMS

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Single cell organisms can surprisingly exceed the number of human protein-coding genes, which are thus not at the origin of the complexity of an organism. In contrast, the relative amount of non-protein-coding sequences increases consistently with organismal complexity. Moreover, the mammalian transcriptome predominantly comprises non-(protein)-coding RNAs (ncRNA), of which the long ncRNAs (lncRNAs) constitute the most abundant part. lncRNAs are highly species- and tissue-specific with very versatile modes of action in accordance with their binding to a large spectrum of molecules and their diverse localization. lncRNAs are transcriptional regulators adding an additional regulatory layer in biological processes and pathophysiological conditions. Here, we review lncRNAs affecting metabolic organs with a focus on the liver, pancreas, skeletal muscle, cardiac muscle, brain, and adipose organ. In addition, we will discuss the impact of lncRNAs on metabolic diseases such as obesity and diabetes. In contrast to the substantial number of lncRNA loci in the human genome, the functionally characterized lncRNAs are just the tip of the iceberg. So far, our knowledge concerning lncRNAs in energy homeostasis is still in its infancy, meaning that the rest of the iceberg is a treasure chest yet to be discovered.

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“…They modulate the gene expression at posttranscriptional or transcriptional level. [22][23][24][25][26] LincR-NA-p21 is a novel lncRNA, which was identified as one direct transcriptional target gene of p53. [18][19][20][21] Moreover, lncRNAs were involved in many cell biology functions, such as cell metastasis, apoptosis, development, proliferation, infiltration, and metabolism.…”

Section: Introductionmentioning

confidence: 99%

LincRNA‐p21 enhances the sensitivity of radiotherapy for gastric cancer by targeting the β‐catenin signaling pathway

Chen

Yuan

Yang

et al. 2018

J of Cellular Biochemistry

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Long noncoding RNAs (lncRNAs) are a large and diverse class of transcribed RNA molecules with a length of more than 200 nucleotides that modulate the gene expression at the posttranscriptional or transcriptional level. LncRNAs played crucial roles in many biological processes, such as cell proliferation, metastasis, and migraton. In this study, we evaluated the role of lincRNA‐p21 in the gastric cancer (GC). We demonstrated that the expression level of lincRNA‐p21 was downregulated in the GC tissues and cell lines. Moreover, ectopic expression of lincRNA‐p21 suppressed the GC cell growth, cell cycle, and migration. Furthermore, we demonstrated that the X‐ray increased the expression level of lincRNA‐p21 in both the HCG‐27 and SGC7901 cells and elevated expression of lincRNA‐p21 increased the radiotherapy sensitivity of the GC cell. In addition, we showed that ectopic expression of lincRNA‐p21 suppressed the β‐catenin and c‐myc expression. Overexpression of lincRNA‐p21 inhibited the GC cell proliferation and increased the radiosensitivity of GC cells by regulating the β‐catenin signaling pathway. These data suggested that lincRNA‐p21 acted as a tumor suppressor gene in the development of GC.

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Pioglitazone up-regulates long non-coding RNA MEG3 to protect endothelial progenitor cells via increasing HDAC7 expression in metabolic syndrome

Cited by 32 publications

References 27 publications

Role of free fatty acids in endothelial dysfunction

Role of free fatty acids in endothelial dysfunction

Long Non-Coding RNAs in Metabolic Organs and Energy Homeostasis

LincRNA‐p21 enhances the sensitivity of radiotherapy for gastric cancer by targeting the β‐catenin signaling pathway

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