miR-101a and miR-30b contribute to inflammatory cytokine-mediated β-cell dysfunction

Zheng, Ying; Wang, Zhen; Tu, Yiting; Shen, Hongwei; Dai, Zhijie; Lin, Jian; Zhou, Zhiguang

doi:10.1038/labinvest.2015.112

Cited by 69 publications

(59 citation statements)

References 35 publications

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“…For example, Belgard et al show that overexpression of the miR-200 family in mice is sufficient to induce β-cell apoptosis and lethal T2DM through indirect activation of the pro-apoptotic genes Trp53 and Bax [12], while elevated miR-34a promotes MIN6 cell apoptosis by directly binding to the 3’-UTR of the anti-apoptotic gene Bcl-2 [13]. …”

Section: Mirnas and Pancreatic β-Cellsmentioning

confidence: 99%

Regulatory Roles of MicroRNAs in Diabetes

Feng

Xing

Xie

2016

IJMS

128

100

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MicroRNAs (miRNAs), a class of endogenous small noncoding RNAs in eukaryotes, have been recognized as significant regulators of gene expression through post-transcriptional mechanisms. To date, >2000 miRNAs have been identified in the human genome, and they orchestrate a variety of biological and pathological processes. Disruption of miRNA levels correlates with many diseases, including diabetes mellitus, a complex multifactorial metabolic disorder affecting >400 million people worldwide. miRNAs are involved in the pathogenesis of diabetes mellitus by affecting pancreatic β-cell functions, insulin resistance, or both. In this review, we summarize the investigations of the regulatory roles of important miRNAs in diabetes, as well as the potential of circulating miRNAs as diagnostic markers for diabetes mellitus.

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Section: Mirnas and Pancreatic β-Cellsmentioning

confidence: 99%

Regulatory Roles of MicroRNAs in Diabetes

Feng

Xing

Xie

2016

IJMS

128

100

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“…Several recent studies have indicated a role for miRNAs in the regulation of autoimmunity progression and diabetes development (20–23), including the regulation of inflammatory cytokine-mediated β-cell dysfunction and death (24–26). Additionally, there may be a link between miRNAs and regulation of T1D candidate genes (27) and β-cell responses to viral infection (28).…”

Section: Introductionmentioning

confidence: 99%

MicroRNAs miR-23a-3p, miR-23b-3p, and miR-149-5p Regulate the Expression of Proapoptotic BH3-Only Proteins DP5 and PUMA in Human Pancreatic β-Cells

et al. 2016

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Type 1 diabetes (T1D) is an autoimmune disease leading to β-cell destruction. MicroRNAs (miRNAs) are small noncoding RNAs that control gene expression and organ formation. They participate in the pathogenesis of several autoimmune diseases, but the nature of miRNAs contributing to β-cell death in T1D and their target genes remain to be clarified. We performed an miRNA expression profile on human islet preparations exposed to the cytokines IL-1β plus IFN-γ. Confirmation of miRNA and target gene modification in human β-cells was performed by real-time quantitative PCR. Single-stranded miRNAs inhibitors were used to block selected endogenous miRNAs. Cell death was measured by Hoechst/propidium iodide staining and activation of caspase-3. Fifty-seven miRNAs were detected as modulated by cytokines. Three of them, namely miR-23a-3p, miR-23b-3p, and miR-149-5p, were downregulated by cytokines and selected for further studies. These miRNAs were found to regulate the expression of the proapoptotic Bcl-2 proteins DP5 and PUMA and consequent human β-cell apoptosis. These results identify a novel cross talk between a key family of miRNAs and proapoptotic Bcl-2 proteins in human pancreatic β-cells, broadening our understanding of cytokine-induced β-cell apoptosis in early T1D.

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“…97 In our previous study, we found that IL-1β treatment induced increased miR-101a and miR-30b expression in β-cells and that the two miRNAs contributed to cytokinemediated β-cell apoptosis and dysfunction. 98 miR-101a and miR-30b downregulate proinsulin expression and reduce the insulin content via direct suppression of the transcriptional factor Neurod1. Furthermore, miR-101a/miR-30b-mediated β-cell apoptosis is related to decreased Bcl2 expression.…”

Section: Mirnas: Participants In Autoimmunity-mediated β-Cell Damagementioning

confidence: 99%

“…We also showed that miR-101a impaired GSIS by inhibiting Onecut2. 98 Recently, Grieco et al reported that miR-23a, miR-23b and miR-149 were downregulated upon exposure of β-cells to the proinflammatory cytokines IL-1β+IFN-γ. These downregulated miRNAs were further demonstrated to modulate the expression levels of the pro-apoptotic Bh3-only proteins Dp5 and Puma, consequently affecting β-cell apoptosis.…”

Section: Mirnas: Participants In Autoimmunity-mediated β-Cell Damagementioning

confidence: 99%

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miRNAs: novel regulators of autoimmunity-mediated pancreatic β-cell destruction in type 1 diabetes

2017

Self Cite

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MicroRNAs (miRNAs) are a series of conserved, short, non-coding RNAs that modulate gene expression in a posttranscriptional manner. miRNAs are involved in almost every physiological and pathological process. Type 1 diabetes (T1D) is an autoimmune disease that is the result of selective destruction of pancreatic β-cells driven by the immune system. miRNAs are also important participants in T1D pathogenesis. Herein, we review the most recent data on the potential involvement of miRNAs in T1D. Specifically, we focus on two aspects: the roles of miRNAs in maintaining immune homeostasis and regulating β-cell survival and/or functions in T1D. We also discuss circulating miRNAs as potent biomarkers for the diagnosis and prediction of T1D and investigate potential therapeutic approaches for this disease.

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miR-101a and miR-30b contribute to inflammatory cytokine-mediated β-cell dysfunction

Cited by 69 publications

References 35 publications

Regulatory Roles of MicroRNAs in Diabetes

Regulatory Roles of MicroRNAs in Diabetes

MicroRNAs miR-23a-3p, miR-23b-3p, and miR-149-5p Regulate the Expression of Proapoptotic BH3-Only Proteins DP5 and PUMA in Human Pancreatic β-Cells

miRNAs: novel regulators of autoimmunity-mediated pancreatic β-cell destruction in type 1 diabetes

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