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Single-cell RNA sequencing of zebrafish pancreatic cells during beta-cell regeneration

ABSTRACT: Single-cell RNA sequencing of zebrafish pancreatic cells during beta-cell regeneration

PROVIDER: PRJNA699078 | ENA |

REPOSITORIES: ENA

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Single-cell RNA sequencing of zebrafish pancreatic cells during beta-cell regeneration

Project description:To better understand the underlying mechanism of beta-cell regeneration in adult zebrafish, we performed single-cell transcriptomic profiling of the pancreatic tissue (using 10X Genomics) at various stages post beta-cell ablation.

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Project description:We aimed to understand the functional roles of islet cellular oscillators under diabetic conditions and during β-cell regeneration. We assessed diurnal regulation of β-cell proliferation and the transcriptional landscape in α- and residual β-cells following β-cell ablation in Insulin-rtTA/TET-DTA mice that simultaneously expressed α- and β-cell specific fluorescent reports. The mouse pancreatic islets were isolated over 24-h with 4-h interval, followed by separation of α- and β- cells using FACS sorting, RNA extraction and RNA sequencing. Acute hyperglycemia and loss of β-cell mass perturbed absolute expression levels and temporal transcriptome profiles in residual β-cells, whereas in neighboring α-cells only changes in temporal profiles were observed. Strikingly, compensatory regeneration of β-cells exhibited circadian rhythmicity. In arrhythmic Bmal1 deficient mice, massive β-cell ablation led to aggravated hyperglycemia, hyperglucagonemia and a fatal diabetes. No compensatory proliferation of β-cells was observed in arrhythmic mice, suggesting an essential role of circadian clocks in β-cell regeneration.

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Adiponectin improves local lipid metabolism in regenerating pancreatic islets after β-cell ablation

Project description:Pathways that stimulate β-cell regeneration remain of great clinical interest, yet effective therapeutic avenues that promote survival or reconstitution of β-cell mass remain elusive. Utilizing a mouse model with inducible β-cell apoptosis followed by adiponectin-mediated regeneration, we aimed to identify key molecules boosting β-cell viability. Within the regenerating pancreatic islets, we examined changes within the transcriptome, and observed an extensive upregulation of genes encoding proteins involved in lipid transport and metabolism. The most prominent targets were further confirmed by quantitative PCR and immunofluorescence. Among the upstream regulators predicted by pathway analysis of the transcriptome, we detected enhanced levels of two key transcription factors, HNF4α and PPARα. Enhanced leptin levels in circulation may also contribute to the anti-lipotoxic program in islets. In summary, our data suggest that improving local lipid metabolism as an important anti-lipotoxic phenomenon to boost β-cell regeneration, primarily mediated by adiponectin’s action on the β-cells directly as well as on the adipocyte. RNA profiles of pancreatic islets isolated from PANIC-ATTAT mice crossed with adiponectin wild-type (P-Adn+/+) or the overexpressing transgene (P-AdnTg/+) at 5 weeks after initial dimerizer administration.

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