The GluCre‐ROSA26EYFP mouse: A new model for easy identification of living pancreatic α‐cells

Quoix, Nicolas; Cheng-Xue, Rui; Guiot, Yves; Herrera, Pedro Luis; Henquin, Jean‐Claude; Gilon, Patrick

doi:10.1016/j.febslet.2007.07.068

Cited by 82 publications

(95 citation statements)

References 32 publications

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“…For liver timeseries experiments, livers were isolated from CD1 mice, stored overnight at 4°C in RNAlater (Ambion), and then stored at À80°C. Mouse pure beta-cells were purified from islets of RIPYY mice expressing EYFP under the rat insulin promoter, i.e., specifically in beta-cells (Quoix et al 2007). Additional details on tissue preparation and RNA extraction are provided in the Supplemental Material.…”

Section: Methods Preparation Of Tissues and Purified Cellsmentioning

confidence: 99%

Tissue-specific disallowance of housekeeping genes: The other face of cell differentiation

Thorrez¹,

Laudadio²,

Deun³

et al. 2010

Genome Res.

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179

206

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We report on a hitherto poorly characterized class of genes that are expressed in all tissues, except in one. Often, these genes have been classified as housekeeping genes, based on their nearly ubiquitous expression. However, the specific repression in one tissue defines a special class of “disallowed genes.” In this paper, we used the intersection-union test to screen for such genes in a multi-tissue panel of genome-wide mRNA expression data. We propose that disallowed genes need to be repressed in the specific target tissue to ensure correct tissue function. We provide mechanistic data of repression with two metabolic examples, exercise-induced inappropriate insulin release and interference with ketogenesis in liver. Developmentally, this repression is established during tissue maturation in the early postnatal period involving epigenetic changes in histone methylation. In addition, tissue-specific expression of microRNAs can further diminish these repressed mRNAs. Together, we provide a systematic analysis of tissue-specific repression of housekeeping genes, a phenomenon that has not been studied so far on a genome-wide basis and, when perturbed, can lead to human disease.

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Section: Methods Preparation Of Tissues and Purified Cellsmentioning

confidence: 99%

Tissue-specific disallowance of housekeeping genes: The other face of cell differentiation

Thorrez¹,

Laudadio²,

Deun³

et al. 2010

Genome Res.

Self Cite

179

206

View full text Add to dashboard Cite

show abstract

“…Indeed, it has been proposed that a pro-α cell population exists as a facultative progenitor that exhibits features of β and α cells in mammals (Habener and Stanojevic, 2012), although this proposition contradicts earlier lineage-tracing studies (Herrera, 2000) that showed that mature β and α cells arise from distinct lineages. As ∼20-65% of α cells are not marked in glucagon:Cre transgenic mice (Herrera, 2000;Quoix et al, 2007;Magnuson and Osipovich, 2013;Mastracci et al, 2013), it is possible that relevant subpopulations of α cells have gone undetected in these studies. The development of novel mouse and zebrafish transgenic strains in which Cre is more faithfully regulated by the endogenous glucagon locus might shed light on this possibility.…”

Section: Discussionmentioning

confidence: 99%

glucagon is essential for alpha cell transdifferentiation and beta cell neogenesis

et al. 2015

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The interconversion of cell lineages via transdifferentiation is an adaptive mode of tissue regeneration and an appealing therapeutic target. However, its clinical exploitation is contingent upon the discovery of contextual regulators of cell fate acquisition and maintenance. In murine models of diabetes, glucagon-secreting alpha cells transdifferentiate into insulin-secreting beta cells following targeted beta cell depletion, regenerating the form and function of the pancreatic islet. However, the molecular triggers of this mode of regeneration are unknown. Here, using lineage-tracing assays in a transgenic zebrafish model of beta cell ablation, we demonstrate conserved plasticity of alpha cells during islet regeneration. In addition, we show that glucagon expression is upregulated after injury. Through gene knockdown and rescue approaches, we also find that peptides derived from the glucagon gene are necessary for alpha-to-beta cell fate switching. Importantly, whereas beta cell neogenesis was stimulated by glucose, alpha-to-beta cell conversion was not, suggesting that transdifferentiation is not mediated by glucagon/GLP-1 control of hepatic glucose production. Overall, this study supports the hypothesis that alpha cells are an endogenous reservoir of potential new beta cells. It further reveals that glucagon plays an important role in maintaining endocrine cell homeostasis through feedback mechanisms that govern cell fate stability.

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“…Several factors may explain this lack of information about glucagon secretion. First, the scarcity of this cell population in islets of animal models such as mice and rats along with several technical limitations of conventional methods have made it more difficult to study a-cells than b-cells (Quoix et al 2007). Second, the lack of functional identification patterns has also been an important limitation in a-cell research.…”

Section: Introductionmentioning

confidence: 99%

Physiology of the pancreatic α-cell and glucagon secretion: role in glucose homeostasis and diabetes

Quesada¹,

Tudurí²,

Ripoll³

et al. 2008

Journal of Endocrinology

336

330

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The secretion of glucagon by pancreatic a-cells plays a critical role in the regulation of glycaemia. This hormone counteracts hypoglycaemia and opposes insulin actions by stimulating hepatic glucose synthesis and mobilization, thereby increasing blood glucose concentrations. During the last decade, knowledge of a-cell physiology has greatly improved, especially concerning molecular and cellular mechanisms. In this review, we have addressed recent findings on a-cell physiology and the regulation of ion channels, electrical activity, calcium signals and glucagon release. Our focus in this review has been the multiple control levels that modulate glucagon secretion from glucose and nutrients to paracrine and neural inputs. Additionally, we have described the glucagon actions on glycaemia and energy metabolism, and discussed their involvement in the pathophysiology of diabetes. Finally, some of the present approaches for diabetes therapy related to a-cell function are also discussed in this review. A better understanding of the a-cell physiology is necessary for an integral comprehension of the regulation of glucose homeostasis and the development of diabetes.

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The GluCre‐ROSA26EYFP mouse: A new model for easy identification of living pancreatic α‐cells

Cited by 82 publications

References 32 publications

Tissue-specific disallowance of housekeeping genes: The other face of cell differentiation

Tissue-specific disallowance of housekeeping genes: The other face of cell differentiation

glucagon is essential for alpha cell transdifferentiation and beta cell neogenesis

Physiology of the pancreatic α-cell and glucagon secretion: role in glucose homeostasis and diabetes

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