MicroRNA-19b downregulates insulin 1 through targeting transcription factor NeuroD1

Zhang, Zhenwu; Zhang, Liqiang; Lei, Ding; Wang, Fa; Sun, Yanjun; An, Yang; Zhao, Ye; Li, Yuhua; Teng, Chun‐Bo

doi:10.1016/j.febslet.2011.06.039

Cited by 52 publications

(37 citation statements)

References 37 publications

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“…Rfx6 , another Ngn3-dependent gene in endocrine cells, is under tight regulation by two glucose-regulated miRNAs, miR-30d and let-7e (Liao et al, 2013). Others have shown that miR-19b represses insulin gene transcription following engagement of its mRNA target NeuroD1 (Zhang et al, 2011). Nevertheless, a role for miR-19b, miR-30d, and let-7e during β-cell development remains to be demonstrated.…”

Section: Mirnas and The Acquisition Of β-Cell Identitymentioning

confidence: 99%

“…Specific miRNAs affect insulin production (Melkman-Zehavi et al, 2011; Zhang et al, 2011; Nieto et al, 2012; Setyowati Karolina et al, 2013; Xu et al, 2015), insulin exocytosis (Plaisance et al, 2006; Lovis et al, 2008a), growth (Tattikota et al, 2014), or apoptosis (Lovis et al, 2008b; Ruan et al, 2011). Additionally, to the best of our knowledge, the function of only four miRNAs (miR-375, miR-7a, miR-184, and the miR-200 family) has been addressed in vivo in the β-cell using mouse genetic studies (Poy et al, 2009; Latreille et al, 2014; Tattikota et al, 2014; Belgardt et al, 2015).…”

Section: Role Of Mirnas In Maintaining Mature β-Cell Identitymentioning

confidence: 99%

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MiRNAs in β-Cell Development, Identity, and Disease

2017

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Pancreatic β-cells regulate glucose metabolism by secreting insulin, which in turn stimulates the utilization or storage of the sugar by peripheral tissues. Insulin insufficiency and a prolonged period of insulin resistance are usually the core components of type 2 diabetes (T2D). Although, decreased insulin levels in T2D have long been attributed to a decrease in β-cell function and/or mass, this model has recently been refined with the recognition that a loss of β-cell “identity” and dedifferentiation also contribute to the decline in insulin production. MicroRNAs (miRNAs) are key regulatory molecules that display tissue-specific expression patterns and maintain the differentiated state of somatic cells. During the past few years, great strides have been made in understanding how miRNA circuits impact β-cell identity. Here, we review current knowledge on the role of miRNAs in regulating the acquisition of the β-cell fate during development and in maintaining mature β-cell identity and function during stress situations such as obesity, pregnancy, aging, or diabetes. We also discuss how miRNA function could be harnessed to improve our ability to generate β-cells for replacement therapy for T2D.

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Section: Mirnas and The Acquisition Of β-Cell Identitymentioning

confidence: 99%

Section: Role Of Mirnas In Maintaining Mature β-Cell Identitymentioning

confidence: 99%

MiRNAs in β-Cell Development, Identity, and Disease

2017

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“…The MIN6 insulinoma cells were maintained in DMEM containing 25 mmol/L glucose supplemented with 15% FBS and 50 μmol/L 2-mercaptoethanol. Isolation of adult pancreatic progenitor cells was described in our previous report [20]. Pancreatic progenitor cells were cultured with DMEM/F12 medium containing 2% FBS and supplemented with 1×B27 (Invitrogen), 20 ng/mL EGF (R&D), 10 ug/mL insulin (Sigma-Aldrich) and 50 μmol/L 2-mercaptoethanol (Sigma-Aldrich).…”

Section: Methodsmentioning

confidence: 99%

miR-375 Inhibits Proliferation of Mouse Pancreatic Progenitor Cells by Targeting YAP1

Zhang

Men

Feng

et al. 2013

Cell Physiol Biochem

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Background/Aims: The Hippo signaling pathway regulates expansion and differentiation of stem cells and tissue progenitor cells during organ development and tissue regeneration. Previous studies have shown that YAP1, a potent effector of the Hippo signaling pathway, plays a crucial role in pancreas development, but the function of YAP1 in pancreatic progenitor cells is less known. Methods: The spatio-temporal expression pattern of YAP1 in mouse developing pancreata was detected by in situ hybridization. The effect of silencing YAP1 on the proliferation of pancreatic progenitor cells was analyzed by CCK-8 assay and Ki67 immunostaining. The regulation of miR-375 on YAP1 expression was determined by dual luciferase reporter assay, QRT-PCR and western blot. Finally, the influence of miR-375 on proliferation of pancreatic progenitor cells was analyzed by CCK-8 assay and Ki67 immunostaining. Results: We found that YAP1 was highly expressed in embryonic and adult pancreatic progenitor cells. Knocking down YAP1 by siRNA inhibited the proliferation of pancreatic progenitor cells. The mouse YAP1 was a target gene of miR-375, and miR-375 could target the 3' UTR of YAP1 mRNA to decrease its protein and mRNA levels. Similar to silencing YAP1 by siRNA, the proliferation of pancreatic progenitor cells was inhibited significantly by miR-375. Conclusion: Our results indicate that YAP1 is necessary for the proliferation of pancreatic progenitor cells and miR-375 participates in regulating YAP1 expression during pancreatic progenitor cells differentiation.

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“…In the group of inversely regulated miRNA-mRNA pairs, also three previously reported, edited miRNAs and their targets were found. NEROD1 (neurogenic differentiation 1) is known to be targeted by mmu-miR-19b (Zhang et al 2011), whereas the targets of the reported edited mmu-let-7g and mmumiR-153, HOXA9 (homeobox A9), and SYN2 (synapsin II) are predictions of TargetScan. The predicted target for mmu-miR-153, SYN2, is also predicted to be targeted by mmu-miR-30a-c&e as well as mmu-miR-32, all consistently up-regulated in the double knockout ( Table 2).…”

Section: Changes In Mirna Abundance Affect Potential Target Mrnasmentioning

confidence: 99%

Adenosine deaminases that act on RNA induce reproducible changes in abundance and sequence of embryonic miRNAs

Vesely¹,

Tauber²,

Sedlazeck³

et al. 2012

Genome Res.

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Adenosine deaminases that act on RNA bind double-stranded and structured RNAs and convert adenosines to inosines by hydrolytic deamination. Inosines are recognized as guanosines, and, hence, RNA editing alters the sequence information but also structure of RNAs. Editing by ADARs is widespread and essential for normal life and development. Precursors of miRNAs are abundantly edited by ADARs, but neither the abundance nor the consequences of miRNA editing has been firmly established. Using transgenic mouse embryos that are deficient in the two enzymatically active editing enzymes ADAR and ADARB1, we compare relative frequencies but also sequence composition of miRNAs in these genetically modified backgrounds to wild-type mice by “next-generation sequencing.” Deficiency of ADARB1 leads to a reproducible change in abundance of specific miRNAs and their predicted targets. Changes in miRNA abundance seem unrelated to editing events. Additional deletion of ADAR has surprisingly little impact on the mature miRNA repertoire, indicating that miRNA expression is primarily dependent on ADARB1. A-to-G transitions reflecting A-to-I editing events can be detected at few sites and at low frequency during the early embryonic stage investigated. Again, most editing events are ADARB1-dependent with only few editing sites being specifically edited by ADAR. Besides known editing events in miRNAs, a few novel, previously unknown editing events were identified. Some editing events are located to the seed region of miRNAs, opening the possibility that editing leads to their retargeting.

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MicroRNA-19b downregulates insulin 1 through targeting transcription factor NeuroD1

Cited by 52 publications

References 37 publications

MiRNAs in β-Cell Development, Identity, and Disease

MiRNAs in β-Cell Development, Identity, and Disease

miR-375 Inhibits Proliferation of Mouse Pancreatic Progenitor Cells by Targeting YAP1

Adenosine deaminases that act on RNA induce reproducible changes in abundance and sequence of embryonic miRNAs

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