MicroRNA-200 Is Induced by Thioredoxin-interacting Protein and Regulates Zeb1 Protein Signaling and Beta Cell Apoptosis

Filios, Stephen R.; Xu, Guanlan; Chen, Junqin; Hong, Kyung-Hee; Gu, Jie; Shalev, Anath

doi:10.1074/jbc.m114.592360

Cited by 89 publications

(76 citation statements)

References 39 publications

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“…The induction of miR-204 triggered by TXNIP was found to reduce MafA expression and to cause an impairment in insulin biosynthesis [48]. In contrast, miR-200 overexpression promotes β-cell apoptosis and inhibits epithelial-mesenchymal transition, a process thought to be involved in compensatory β-cell mass expansion [47].…”

Section: Contribution Of Other Mirnas To Compensatory β-Cell Mass Expmentioning

confidence: 99%

“…However, transgenic mice overexpressing miR-802 developed glucose intolerance and insulin resistance, suggesting the involvement of this miRNA in the regulation of glucose homeostasis in vivo [45]. Another group of miRNAs, including miR-204 and miR-200 family members, has been shown to be induced by the Thioredoxin-interacting protein (TXNIP), a cellular redox regulator that is up-regulated in diabetes and triggers β-cell apoptosis [47,48]. The induction of miR-204 triggered by TXNIP was found to reduce MafA expression and to cause an impairment in insulin biosynthesis [48].…”

Section: Contribution Of Other Mirnas To Compensatory β-Cell Mass Expmentioning

confidence: 99%

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MicroRNAs and the functional β cell mass: For better or worse

Guay

Regazzi

2015

Diabetes & Metabolism

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Insulin secretion from pancreatic β-cells plays a central role in the control of blood glucose levels. The amount of insulin released by β-cells is precisely adjusted to match the organism requirements. A number of conditions occurring during life, including pregnancy and obesity, can result in a decrease in the sensitivity of insulin target tissues and in the consequent rise in the insulin needs. To preserve glucose homeostasis, the augmented insulin demand requires a compensatory expansion of the mass of pancreatic β-cells and an increase in their secretory activity. This compensatory process is known to be accompanied by modifications in β-cell gene expression but the molecular mechanisms underlying this phenomenon are still poorly understood. Emerging evidence indicate that at least part of these compensatory events may be orchestrated by changes in the level of a novel class of gene regulators, the microRNAs.Indeed, several of these small non-coding RNAs have either positive or negative impacts on β-cell proliferation and survival. The studies reviewed in this paper suggest that the balance between the actions of these two groups of microRNAs with opposing functional effects determines whether β-cells expand sufficiently to maintain blood glucose levels in the normal range or fail to meet the insulin demand with a consequent progression toward diabetes manifestation. A better understanding of the mechanisms governing the changes in the microRNA profile will open the way for the development of new strategies to prevent and/or treat type 2 and gestational diabetes.

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Section: Contribution Of Other Mirnas To Compensatory β-Cell Mass Expmentioning

confidence: 99%

Section: Contribution Of Other Mirnas To Compensatory β-Cell Mass Expmentioning

confidence: 99%

MicroRNAs and the functional β cell mass: For better or worse

Guay

Regazzi

2015

Diabetes & Metabolism

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“…The proapoptotic and diabetogenic functions of Txnip are associated with the Txnip-mediated changes in miRNAs, such as miR-204 and miR-200. 102,103 Txnip can induce miR-204 expression, which in turn regulates Mafa expression and thus modulates β-cell functions, such as insulin production. 102 In addition, Txnip impairs β-cell functions by inducing miR-200.…”

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

confidence: 99%

“…102 In addition, Txnip impairs β-cell functions by inducing miR-200. 103 miR-200 has been demonstrated to target and decrease Zeb1 and promote β-cell apoptosis. 103 A recent study showed that IFN-γ increased Txnip expression in β-cells via inhibition of miR-17, whereas overexpression of miR-17 alleviated the cytokine effect.…”

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

confidence: 99%

“…103 miR-200 has been demonstrated to target and decrease Zeb1 and promote β-cell apoptosis. 103 A recent study showed that IFN-γ increased Txnip expression in β-cells via inhibition of miR-17, whereas overexpression of miR-17 alleviated the cytokine effect. 104 IFN-γ has been reported to lead to miR-17 degradation, probably due to the effective activation of Ire1α.…”

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

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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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Roles of Noncoding RNAs in Islet Biology

Guay

Jacovetti

Bayazit

et al. 2020

Comprehensive Physiology

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The discovery that most mammalian genome sequences are transcribed to RNA has revolutionized our understanding of the mechanisms governing key cellular processes and of the causes of human diseases, including diabetes mellitus. Pancreatic islet cells were found to contain thousands of noncoding RNAs, including microRNAs, Piwi-associated RNAs, small nucleolar RNAs, tRNAderived fragments, long non-coding RNAs and circular RNAs. While the involvement of microRNAs in islet function and in the etiology of diabetes is now well documented, there is emerging evidence indicating that other classes of non-coding RNAs are also participating in different aspects of islet physiology. The aim of this review will be to provide a comprehensive and updated view of the studies carried out in human samples and rodent models over the last 15 years on the role of non-coding RNAs in the control of α-and β-cell development and function and to highlight the recent discoveries in the field. We will not only describe the role of non-coding RNAs in the control of insulin and glucagon secretion but will also address the contribution of these regulatory molecules in the proliferation and survival of islet cells under physiological and pathological conditions. It is now well established that most cells release part of their non-coding RNAs inside small extracellular vesicles allowing the delivery of genetic material to neighboring or distantly located target cells. The role of these secreted RNAs in cell-to-cell communication between β-cells and other metabolic tissues as well as their potential use as diabetes biomarkers will be discussed.-Circulating non-coding RNAs represent promising biomarkers.

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MicroRNA-200 Is Induced by Thioredoxin-interacting Protein and Regulates Zeb1 Protein Signaling and Beta Cell Apoptosis

Cited by 89 publications

References 39 publications

MicroRNAs and the functional β cell mass: For better or worse

MicroRNAs and the functional β cell mass: For better or worse

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

Roles of Noncoding RNAs in Islet Biology

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