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Endocrine cell type sorting and mature architecture in the islets of Langerhans require expression of Roundabout receptors in β cells

ABSTRACT: Endocrine cell type sorting and mature architecture in the islets of Langerhans require expression of Roundabout receptors in β cells

PROVIDER: PRJNA1151018 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30339936.fastq.gz	Fastqsanger.gz
	SRR30339937.fastq.gz	Fastqsanger.gz
	SRR30339938.fastq.gz	Fastqsanger.gz
	SRR30339939.fastq.gz	Fastqsanger.gz

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Endocrine cell type sorting and mature architecture in the islets of Langerhans require expression of Roundabout receptors in β cells

Project description:The spatial architecture of the islets of Langerhans is hypothesized to facilitate synchronized insulin secretion among β cells, yet testing this in vivo in the intact pancreas is challenging. Robo βKO mice, in which the genes Robo1 and Robo2 are deleted selectively in β cells, provide a unique model of altered islet spatial architecture without loss of β cell differentiation or islet damage from diabetes. Combining Robo βKO mice with intravital microscopy, we show here that Robo βKO islets have reduced synchronized intra-islet Ca2+ oscillations among β cells in vivo. We provide evidence that this loss is not due to a β cell-intrinsic function of Robo, mis-expression or mis-localization of Cx36 gap junctions, or changes in islet vascularization or innervation, suggesting that the islet architecture itself is required for synchronized Ca2+ oscillations. These results have implications for understanding structure-function relationships in the islets during progression to diabetes as well as engineering islets from stem cells.

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Endocrine cell type sorting and mature architecture in the islets of Langerhans require expression of Roundabout receptors in β cells.

Project description: Not available

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Deamidation in human islets of Langerhans

Project description:The β-cell plays a central role in the pathogenesis of T1D by neoantigen formation due to the generation of post-translational modifications, such as deamidation, being potential triggers for breaking immune tolerance. We report the detection by LC-MS/MS of 16 novel Gln and 27 novel Asn deamidations in 14 T1D-related proteins in inflammatory cytokine-stressed human islets of Langerhans. T-cell clones responsive against two Gln and three Asn deamidated peptides could be isolated from peripheral blood of T1D subjects. Ex vivo tetramer assays indicated higher T-cell frequencies in subjects with T1D compared to control subjects and a positive correlation between frequencies and insulin antibody levels at diagnosis and duration of disease for one Gln and two Asn deamidated peptides. These results highlight that inflammatory cytokine-exposed human islets are prone to both enzymatic and biochemical deamidation and suggest that both Gln and Asn deamidated peptides can promote the activation of CD4+ T cells in individuals with T1D. These findings add to the growing list of evidence that post-translational modifications undermine tolerance in T1D and may open the road for the development of new diagnostic and therapeutic applications for people living with T1D.

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Epigenetic changes in Langerhans islets preceding the onset of diabetes

Project description:Diabetes-resistant and diabetes-prone female New Zealand Obese mice were classified based on liver fat content and early blood glucose concentrations at 10 weeks of age before the onset of T2D. By using transcriptome and DNA methylome analysis of Langerhans islets, we identified early epigenetic alteration in mice and humans which could serve as putative epigenetic biomarkers

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Transcription profiling of Langerhans cells isolated from CD11c-Cre x Dicer wt/wt and Dicer fl/fl mice to investigate Dicer-dependent miRNA deficiency

Project description:Transcriptional profiling of Langerhans cells isolated from CD11c-Cre x Dicer wt/wt (Dicer +/+ ) and CD11c-Cre x Dicer fl/fl (Dicer-/-) mice. Langerhans cells are isolated via enzymatic digestion of skin followed by antibody staining and FACS sorting

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Project description:To define genetic pathways that regulate development of the endocrine pancreas, we generated transcriptional profiles of enriched cells isolated from four biologically significant stages of endocrine pancreas development: endoderm before pancreas specification, early pancreatic progenitor cells, endocrine progenitor cells and adult islets of Langerhans. These analyses implicate new signaling pathways in endocrine pancreas development, and identified sets of known and novel genes that are temporally regulated, as well as genes that spatially define developing endocrine cells from their neighbors. The differential expression of several genes from each time point was verified by RT-PCR and in situ hybridization. Moreover, we present preliminary functional evidence suggesting that one transcription factor encoding gene (Myt1), which was identified in our screen, is expressed in endocrine progenitors and may regulate alpha, beta and delta cell development. In addition to identifying new genes that regulate endocrine cell fate, this global gene expression analysis has uncovered informative biological trends that occur during endocrine differentiation.

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