The effects of YTHDC1 on islet β-cell function
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA862619 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20662436_1.fastq.gz | Fastqsanger.gz | |||
| SRR20662436_2.fastq.gz | Fastqsanger.gz | |||
| SRR20662437_1.fastq.gz | Fastqsanger.gz | |||
| SRR20662437_2.fastq.gz | Fastqsanger.gz | |||
| SRR20662438_1.fastq.gz | Fastqsanger.gz |
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Project description:The goal of this study is to investigate how YTHDC1 regulates islet β-cell function. Our study represents the first detailed analysis of islet transcriptomes from Ythdc1flox/flox and Ythdc1-βKO mice, generated by RNA-seq technology. The RNA-seq analysis showed that 2869 genes were downregulated and 2825 genes were upregulated in the pancreatic islets of Ythdc1-βKO mice.
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Project description:We measured changes in the human islet proteome following 72-hr exposure to 3 mM R-beta-hydroxybutyrate. Islets from 12 metabolically healthy human islet donors were obtained from the Alberta Diabetes Institute Islet Core
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Project description:Purpose: The goal of this study is to investigate how METTL3 regulates islet β-cell function. Methods: Total RNA was extracted using Tripure Isolation Reagent (Roche, Mannheim, Germany) from pancreatic islets of Mettl3flox/flox and β-Mettl3-KO mice at 8 weeks old. Each RNA sample was pooled from four Mettl3flox/flox and β-Mettl3-KO mice, respectively. Three independent biological replicates for each group were used for RNA-seq. RNA-seq was performed by deep sequencing using an Illumina Novaseq 6000 platform. Paired-end clean reads were aligned to the mouse reference genome(GRCm38.p6) with Hisat2 v2.0.5, and the aligned reads were used to quantify mRNA expression by using featureCounts v1.5.0-p3. Conclusion: Our study represents the first detailed analysis of islet transcriptomes from Mettl3flox/flox and β-Mettl3-KO mice, generated by RNA-seq technology. The RNA-seq analysis showed that 2560 genes were downregulated and 3408 genes were upregulated in the pancreatic islets of β-Mettl3-KO mice. GO analysis showed that the downregulated genes were primarily related to insulin secretion, SNARE binding, and mitochondrial respiratory chain, whereas the upregulated genes were associated with the immune response, B cell activation, and antigen binding.
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Project description:Altered islet architecture is associated with β cell dysfunction and Type 2 Diabetes (T2D) progression, but molecular effectors of islet spatial organization remain mostly unknown. Although Notch signaling is known to regulate pancreatic development, we observed “re-activated” β cell Notch activity in obese mouse models. To test the repercussions and reversibility of Notch effects, we generated doxycycline-dependent, β cell-specific Notch gain-of-function mice. As predicted, we found that Notch activation in post-natal β cells impaired glucose stimulated insulin secretion (GSIS) and glucose intolerance, but we observed a surprising remnant glucose intolerance after doxycycline withdrawal and cessation of Notch activity, associated with a marked disruption of normal islet architecture. Transcriptomic screening of Notch-active islets revealed increased Ephrin signaling. Commensurately, exposure to Ephrin ligands increased β cell repulsion, and impaired murine and human pseudo-islet formation. Consistent with our mouse data, Notch and Ephrin signaling are increased in metabolically-inflexible β cells in patients with T2D. These studies suggest than islet architecture can be permanently altered by β cell Notch/Ephrin signaling during a morphogenetic window in early life.
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Project description:The goal of this study is to investigate how WTAP regulates islet β-cell function. Islets were isolated from pancreatic islets of Wtapflox/flox and Wtap-βKO mice at 7 weeks old. One islet sample was combined from three mice. Total RNA was extracted using Tripure Isolation Reagent (Roche, Mannheim, Germany). Three independent biological replicates for each group were used for RNA-seq. RNA-seq was performed by deep sequencing using an Illumina Novaseq 6000 platform. Paired-end clean reads were aligned to the mouse reference genome(GRCm38/mm10) with Hisat2 v2.0.5, and the aligned reads were used to quantify mRNA expression by using featureCounts v1.5.0-p3. Our study represents the first detailed analysis of islet transcriptomes from Wtapflox/flox and Wtap-βKO mice, generated by RNA-seq technology. The RNA-seq analysis showed that 3015 genes were downregulated and 2900 genes were upregulated in the pancreatic islets of Wtap-βKO mice.
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Project description:Inflammation is a key component of the pathogenesis of obesity-associated type 2 diabetes (T2D). However, the nature of T2D-associated islet inflammation and its impacts on T2D-associated beta cell abnormalities remain poorly defined. Using both diet-induced and genetically modified T2D animal models, we explore immune components of islet inflammation and define their roles in regulating beta cell function and proliferation. Our studies show that T2D-associated islet inflammation is uniquely dominated by macrophages, without the involvement of adaptive immune cells. We identify two islet macrophage populations, characterized by their distinct phenotypes, anatomical distributions and functional properties. Obesity induces a local expansion of intra-islet macrophages, independent of the replenishment from circulating monocytes. In contrast, the abundance of peri-islet macrophages is negligibly affected by obesity. Functionally, intra-islet macrophages impair beta cell function in a cell-cell contact dependent manner. In contrast, both intra- and peri-islet macrophage populations are able to promote beta cell proliferation. Together, these data provide a definitive view of the genesis of T2D-associated islet inflammation and define specific roles of islet macrophages in regulating beta cell function and proliferation.
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Project description:Deterioration of functional islet β-cell mass is the final step in progression to Type 2 diabetes. We previously reported that overexpression of Nkx6.1 in rat islets has the dual effects of enhancing glucose-stimulated insulin secretion (GSIS) and increasing β-cell replication. Here we show that Nkx6.1 strongly upregulates the prohormone VGF in rat islets and that VGF is both necessary and sufficient for Nkx6.1-mediated enhancement of GSIS. Moreover, the VGF-derived peptide TLQP-21 potentiates GSIS in rat and human islets and improves glucose tolerance in vivo. Chronic injection of TLQP-21 in pre-diabetic ZDF rats preserves islet mass and slows diabetes onset. TLQP-21 prevents islet cell apoptosis by a pathway similar to that used by GLP-1, but independent of the GLP-1, GIP, or VIP receptors. Unlike GLP-1, TLQP-21 does not inhibit gastric emptying or increase heart rate. We conclude that a TLQP-21 is a novel agent for enhancing islet β-cell survival and function. We utilized a “sample x reference” experimental design strategy in which RNA extracted from rat pancreatic islets was hybridized to the microarray slide in the presence of labeled rat reference RNA (RRR, Stratagene, LaJolla, CA). Cultures were treated with adenoviruses expressing either the hamster form of Nkx6.1, the mouse form of Pdx1, or the beta-galactosidase enzyme. 3-5 biological replicates each representing independent islet isolations were used for microarray analysis. Briefly, five hundred nanograms of total RNA were used for gene expression profiling following reverse transcription and T-7 polymerase-mediated amplification/labeling with Cyanine-5. Labeled subject cRNA was co-hybridized to Operon rat 27K oligonucleotide arrays with equimolar amounts of Cyanine-3 labeled RRR. Slides were hybridized, washed, and scanned on a Gene Pix 5000 microarray scanner.
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