Long noncoding RNA-MEG3 is involved in diabetes mellitus-related microvascular dysfunction

Qiu, Gui-Zhen; Tian, Wei; Fu, Hua; Li, Chaopeng; Liu, Ban

doi:10.1016/j.bbrc.2016.01.164

Cited by 172 publications

(144 citation statements)

References 29 publications

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“…MEG3 levels are down-regulated in type 1 and type 2 diabetic mice, and the inactivation of MEG3 in normal mice causes decreased insulin synthesis and secretion [38]. Furthermore, MEG3 is down-regulated in diabetic retinas and in retinal endothelial cells upon high glucose stress, which is mediated by the activation of PI3k/Akt signaling [13]. We also found a down-regulation of MEG3 in the DM group, and this evidence suggests potential roles for MEG3 in the pathological processes of diabetes.…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 99%

“…Human beta cell transcriptome analyses uncovered lncRNAs that were tissue-specific, dynamically regulated, and abnormally expressed in type 2 diabetes [10]. Moreover, MIAT and PVT1 were found to mediate high glucose-induced renal injury [11,12], MEG3 was involved in diabetic microvascular dysfunction [13], and the aberrant expression of MALAT1 was found both in diabetic retinopathy and cardiomyopathy [14,15].…”

mentioning

confidence: 99%

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Microarray Analysis of Long Noncoding RNAs in Female Diabetic Peripheral Neuropathy Patients

Lin

Cai

et al. 2018

Cell Physiol Biochem

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Background/Aims: Diabetic peripheral neuropathy (DPN) is the most common complication of diabetes mellitus (DM). Because of its controversial pathogenesis, DPN is still not diagnosed or managed properly in most patients. Methods: In this study, human lncRNA microarrays were used to identify the differentially expressed lncRNAs in DM and DPN patients, and some of the discovered lncRNAs were further validated in additional 78 samples by quantitative realtime PCR (qRT-PCR). Results: The microarray analysis identified 446 and 1327 differentially expressed lncRNAs in DM and DPN, respectively. The KEGG pathway analysis further revealed that the differentially expressed lncRNA-coexpressed mRNAs between DPN and DM groups were significantly enriched in the MAPK signaling pathway. The lncRNA/mRNA coexpression network indicated that BDNF and TRAF2 correlated with 6 lncRNAs. The qRT-PCR confirmed the initial microarray results. Conclusion: These findings demonstrated that the interplay between lncRNAs and mRNA may be involved in the pathogenesis of DPN, especially the neurotrophin-MAPK signaling pathway, thus providing relevant information for future studies.

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Section: Cellular Physiology and Biochemistrymentioning

confidence: 99%

mentioning

confidence: 99%

Microarray Analysis of Long Noncoding RNAs in Female Diabetic Peripheral Neuropathy Patients

Lin

Cai

et al. 2018

Cell Physiol Biochem

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“…In contrast to lncRNA MIAT, lncRNA MEG3 (maternally expressed gene 3) expression was significantly downregulated in the retinas and endothelial cells of STZ-induced diabetic mice upon high glucose and oxidative stress conditions [94]. Its knockdown regulated retinal endothelial cell proliferation, migration, and tube formation in vitro .…”

Section: Lncrna In Diabetes and Pancreatic Function/glucose Homeosmentioning

confidence: 99%

Long Noncoding RNAs in Metabolic Syndrome Related Disorders

Losko

Kotlinowski

Jura

2016

Mediators of Inflammation

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Ribonucleic acids (RNAs) are very complex and their all functions have yet to be fully clarified. Noncoding genes (noncoding RNA, sequences, and pseudogenes) comprise 67% of all genes and they are represented by housekeeping noncoding RNAs (transfer RNA (tRNA), ribosomal RNA (rRNA), small nuclear RNA (snRNA), and small nucleolar RNA (snoRNA)) that are engaged in basic cellular processes and by regulatory noncoding RNA (short and long noncoding RNA (ncRNA)) that are important for gene expression/transcript stability. In this review, we summarize data concerning the significance of long noncoding RNAs (lncRNAs) in metabolic syndrome related disorders, focusing on adipose tissue and pancreatic islands.

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“…Ballantyne et al (13) demonstrated that smooth muscle enriched lncRNA is involved in regulating the proliferation of VSMCs and is highly expressed in atherosclerotic plaques. Furthermore, Qiu et al (14) revealed that silencing the expression of lncRNA maternally expressed gene 3 (lncRNAMEG3) promotes endothelial cell proliferation and angiogenesis; and upregulation of the expression of lncRNAMEG3 suppresses angiogenesis and the cell cycle in endothelial cells. These results indicate that lncRNAs serve key functions in the regulation of endothelial cell function.…”

Section: Introductionmentioning

confidence: 99%

Effect of silencing lncRNATUG1 on rapamycin‑induced inhibition of endothelial cell proliferation and migration

et al. 2018

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Angiogenesis refers to the formation of new blood vessels from existing blood vessels. The proliferation and migration of endothelial cells serves a key function in this process. Previous research has demonstrated that rapamycin suppresses endothelial cell proliferation and migration, as well as angiogenesis. However, the mechanism by which rapamycin inhibits the proliferation and migration of endothelial cells remains unclear. Long noncoding RNAs (lncRNAs) serve a key function in the regulation of endothelial cell function. The aim of the current study was to investigate whether lncRNA taurine upregulated 1 (lncRNATUG1) is involved in rapamycin-induced inhibition of proliferation and migration in human umbilical vein endothelial cells (HUVECs). Reverse transcription quantitative polymerase chain reaction results indicated that the expression of lncRNATUG1 was upregulated in HUVECs that had been cultured with rapamycin. Subsequently, HUVECs were transfected with siRNAs and CCK-8 assays were performed to detect cell proliferation; additionally, flow cytometry was employed to detect cell apoptosis, and wound healing assays were performed to investigate cell migration. The results demonstrated that rapamycin suppressed the proliferation and migration of HUVECs, and promoted the apoptosis of HUVECs. In addition, rapamycin downregulated the expression of vascular endothelial growth factor (VEGF), matrix metalloproteinase (MMP)-2 and MMP-9 in HUVECs. However, silencing of lncRNATUG1 was revealed to attenuate rapamycin-induced inhibition of cellular proliferation and migration of HUVECs, as well as upregulating the expression of VEGF, MMP2 and MMP-9. These results suggested that lncRNATUG1 regulates rapamycin-induced inhibition of endothelial cell proliferation and migration. Therefore, lncRNATUG1 may serve a key function in rapamycin-induced inhibition of endothelial cell proliferation and migration.

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Long noncoding RNA-MEG3 is involved in diabetes mellitus-related microvascular dysfunction

Cited by 172 publications

References 29 publications

Microarray Analysis of Long Noncoding RNAs in Female Diabetic Peripheral Neuropathy Patients

Microarray Analysis of Long Noncoding RNAs in Female Diabetic Peripheral Neuropathy Patients

Long Noncoding RNAs in Metabolic Syndrome Related Disorders

Effect of silencing lncRNATUG1 on rapamycin‑induced inhibition of endothelial cell proliferation and migration

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