Lnc-ing non-coding RNAs with metabolism and diabetes: roles of lncRNAs

Goyal, Neha; Kesharwani, Devesh; Datta, Malabika

doi:10.1007/s00018-018-2760-9

Cited by 72 publications

(56 citation statements)

References 112 publications

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“…More important, the distinct influence on the biology of vascular cells conferred by lncRNAs has been associated with diabetic vascular complications (Leung, Amaram, & Natarajan, ). A previous study indicated that lncRNAs could serve as biomarkers or therapeutic targets in the treatment of DM and its related complications (Goyal, Kesharwani, & Datta, ). In addition, research has indicated there to be a correlation between highly expressed lncRNA H19 and a host of human cancers, including multiple myeloma, and plays a significant role in the occurrence of cancers (Pan et al, ).…”

Section: Discussionmentioning

confidence: 99%

Retracted: Downregulation of long noncoding RNA H19 rescues hippocampal neurons from apoptosis and oxidative stress by inhibiting IGF2 methylation in mice with streptozotocin‐induced diabetes mellitus

Che

et al. 2018

Journal Cellular Physiology

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The diabetes mellitus (DM)‐induced reduction of neurogenesis in the hippocampus is consequently accompanied by cognitive decline. The present study set out to define the critical role played by long noncoding RNA H19 (lncRNA H19) in the apoptosis of hippocampal neurons, as well as oxidative stress (OS) in streptozotocin (STZ)‐induced DM mice through regulation of insulin‐like growth factor 2 (IGF2) methylation. The expression of lncRNA H19 in the hippocampal neurons and surviving neurons were detected. Hippocampal neurons were cultured and transfected with oe‐H19, sh‐H19, oe‐IGF2, or sh‐IGF2, followed by detection of the expressions of IGF2 and apoptosis‐related genes. Determination of the lipid peroxide and glutathione levels was conducted, while antioxidant enzyme activity was identified. The IGF2 methylation, the binding of lncRNA H19 to DNA methyltransferase, and the binding of lncRNA H19 to IGF2 promoter region were detected. DM mice exhibited high expressions of H19, as well as a decreased hippocampal neurons survival rate. Higher lncRNA H19 expression was found in DM. Upregulated lncRNA H19 significantly increased the expression of Bax and caspase‐3 but decreased that of Bcl‐2, thus promoting the apoptosis of hippocampal neuron. Besides, upregulation of lncRNA H19 induced OS. LncRNA H19 was observed to bind specifically to the IGF2 gene promoter region and promote IGF2 methylation by enriching DNA methyltransferase, thereby silencing IGF2 expression. Taken together, downregulated lncRNA H19 reduces IGF2 methylation and enhances its expression, thereby suppressing hippocampal neuron apoptosis and OS in STZ‐induced (DM) mice.

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Section: Discussionmentioning

confidence: 99%

Retracted: Downregulation of long noncoding RNA H19 rescues hippocampal neurons from apoptosis and oxidative stress by inhibiting IGF2 methylation in mice with streptozotocin‐induced diabetes mellitus

Che

et al. 2018

Journal Cellular Physiology

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“…The differential expression of the selected lncRNAs in vivo reconfirmed the results from the gene array analysis. LncRNAs have been reported to be involved in the process of diabetes development ; our newly discovered lncRNAs may provide new candidates for T2DM study.…”

Section: Introductionmentioning

confidence: 94%

Microarray Profiling and Coexpression Network Analysis of Long Noncoding RNAs in Adipose Tissue of Obesity‐T2DM Mouse

Yao

Liu

et al. 2019

Obesity

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Objective The aim of this study was to understand more about long noncoding RNAs (lncRNAs) as potential prediction biomarkers or therapeutic targets for obesity and type 2 diabetes mellitus (T2DM). This study aimed to find more lncRNA candidates related to obesity and T2DM. Methods In this study, a high‐fat diet (HFD)‐induced obesity‐T2DM mouse model was used, and a mRNA and lncRNA expression map was drawn up in adipose tissue by microarray technology. Then Gene Ontology analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis were performed and revealed that the most associated genes and pathways were metabolism‐related ones. The candidate lncRNA expression was further validated in adipose tissue from HFD‐induced mice by quantitative real‐time polymerase chain reaction analysis. Results Transcriptome analyses were performed to show expression profiles of mRNAs and lncRNAs in epididymal adipose tissue in the obesity‐T2DM mice. A total of 124 lncRNAs and 1,606 mRNAs were differentially expressed between the chow and HFD groups. Then, an mRNA‐lncRNA coexpression network was constructed. Based on a series of analyses, 15 candidate lncRNAs were screened, and their expression was further validated by quantitative real‐time polymerase chain reaction analysis. Conclusions The results reveal significant differences between the transcriptomes of the HFD and control groups in adipose tissue that provide clues to the molecular mechanisms of diet‐induced metabolic disorders as well as biomarkers of risk for these disorders.

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“…In the survey, Roggli et al (2012) investigated the effects of miRNAs on the PBCs dysfunction in NOD animals. They observed that the levels of miR-29a, miR-29b, and miR-29c increased in pancreas islets of NOD animals thru the prediabetic phases and also in the human islets (Goyal et al, 2018). It has been revealed that lncRNAs' effects on gene expression procedure can be performed at the each stage of the transcription, posttranscription and translation.…”

Section: Oxidative Stress and T2dmentioning

confidence: 99%

“…A small portion of these long noncoding RNAs (lncRNAs) have shown to regulate gene expression by some procedures, such as modulation of chromosomal structure, transcription, mRNA transport or translation (St. Laurent, Wahlestedt, & Kapranov, ). Some of the recent investigations have discovered many lncRNAs in β cells of the human Langerhans islets (Goyal, Kesharwani, & Datta, ; Morán et al, ; You et al, ). It has been suggested that β‐cell lncRNAs controlled extracellular concentrations of glucose.…”

Section: Introductionmentioning

confidence: 99%

Molecular aspects of pancreatic β‐cell dysfunction: Oxidative stress, microRNA, and long noncoding RNA

Borujeni

Esfandiary

Baradaran

et al. 2018

Journal Cellular Physiology

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Metabolic syndrome is known as a frequent precursor of type 2 diabetes mellitus (T2D). This disease could affect 8% of the people worldwide. Given that pancreatic β‐cell dysfunction and loss have central roles in the initiation and progression of the disease, the understanding of cellular and molecular pathways associated with pancreatic β‐cell dysfunction can provide more information about the underlying pathways involved in T2D. Multiple lines evidence indicated that oxidative stress, microRNA, and long noncoding RNA play significant roles in various steps of diseases. Oxidative stress is one of the important factors involved in T2D pathogenesis. This could affect the function and survival of the β cell via activation or inhibition of several processes and targets, such as receptor‐signal transduction, enzyme activity, gene expression, ion channel transport, and apoptosis. Besides oxidative stress, microRNAs and noncoding RNAs have emerged as epigenetic regulators that could affect pancreatic β‐cell dysfunction. These molecules exert their effects via targeting a variety of cellular and molecular pathways involved in T2D pathogenesis. Here, we summarized the molecular aspects of pancreatic β‐cell dysfunction. Moreover, we highlighted the roles of oxidative stress, microRNAs, and noncoding RNAs in pancreatic β‐cell dysfunction.

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Lnc-ing non-coding RNAs with metabolism and diabetes: roles of lncRNAs

Cited by 72 publications

References 112 publications

Retracted: Downregulation of long noncoding RNA H19 rescues hippocampal neurons from apoptosis and oxidative stress by inhibiting IGF2 methylation in mice with streptozotocin‐induced diabetes mellitus

Retracted: Downregulation of long noncoding RNA H19 rescues hippocampal neurons from apoptosis and oxidative stress by inhibiting IGF2 methylation in mice with streptozotocin‐induced diabetes mellitus

Microarray Profiling and Coexpression Network Analysis of Long Noncoding RNAs in Adipose Tissue of Obesity‐T2DM Mouse

Molecular aspects of pancreatic β‐cell dysfunction: Oxidative stress, microRNA, and long noncoding RNA

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