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A histological and transcriptional characterization of the pancreatic acinar tissue in type 1 diabetes

ABSTRACT: A histological and transcriptional characterization of the pancreatic acinar tissue in type 1 diabetes

PROVIDER: PRJNA682616 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR13199700.fastq.gz	Fastqsanger.gz
	SRR13199701.fastq.gz	Fastqsanger.gz
	SRR13199702.fastq.gz	Fastqsanger.gz
	SRR13199703.fastq.gz	Fastqsanger.gz

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A histological and transcriptional characterization of the pancreatic acinar tissue in type 1 diabetes

Project description:Despite reduced function and volume of the exocrine pancreas in type 1 diabetes, literature describing the histology and the molecular biological profile in this area is limited. Here, the density of acinar cells was examined adjacent to and at varying distances from islets and the transcriptome was analyzed on laser capture microdissected (LCM) tissue from organ donors with and without type 1 diabetes. We demonstrate preserved acinar nuclei density in type 1 diabetes and find no support of acinar atrophy in pancreata devoid of insulin. The density of acinar nuclei was unaltered in type 1 diabetes. Principal component analysis of the transcriptomes of acinar tissue extracted from various areas of the pancreas showed no apparent clustering based on disease status, and few differentially expressed genes were discovered. However, when performing GSEA, transcriptional alterations were present in the acinar tissue independently of the distance from islets. Two gene sets were enriched in all exocrine regions; Myc Targets V2 and Estrogen Response Early. The alteration of these is a possible link to the increased incidence of pancreatic cancer in type 1 diabetes. Taken together, these new data shed light on the pathogenesis of type 1 diabetes and its involvement of the entire pancreas.

2021-02-19 | GSE162689 | GEO

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Histological and transcriptional characterization of the pancreatic acinar tissue in type 1 diabetes.

Project description:IntroductionDespite a reduced function and volume of the exocrine pancreas in type 1 diabetes, the acinar cells remain understudied in type 1 diabetes research. The hypothesis of this study is that the acinar tissue is altered in subjects with type 1 diabetes compared with subjects without diabetes.Research design and methodsThe cell density, expression of digestive enzymes, and transcriptome of acinar tissue at varying distances from islets were analyzed using histology, immunostaining, and AmpliSeq RNA sequencing of laser capture microdissected tissue. Pancreases examined were from organ donors with or without type 1 diabetes.ResultsWe demonstrate preserved acinar nuclei density and find no support of acinar atrophy in type 1 diabetes. Staining for digestive enzymes (amylase, lipase, and trypsin) demonstrated an evenly distributed expression in the exocrine parenchyma; although occasional amylase-negative regions appeared in tissue that had been formalin-fixed and paraffin-embedded, this phenomenon was not evident in frozen tissue. Gene set enrichment analysis of whole transcriptome data identified transcriptional alterations in type 1 diabetes that were present in the acinar tissue independent of the distance from islets. Among these, the two most enriched gene sets were Myc Targets V2 and Estrogen Response Early.ConclusionTaken together, these new data emphasize the involvement of the entire pancreas in type 1 diabetes pathology. The alteration of the gene sets Myc Targets V2 and Estrogen Response Early is a possible link to the increased incidence of pancreatic cancer in type 1 diabetes.

| S-EPMC8149357 | biostudies-literature

RNA-Seq of explanted murine pancreatic acinar cells

Project description:To investigate the underlying changes during acinar-to-ductal metaplasia, pancreatic acinar cells were isolated from 5 week old KrasG12D-mice. RNA was isolated immediately after isolation (t=0 days) or after 3 days embedded in collagen.

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Epigenetic reprogramming in pancreatic acinar cell in the absence of MIST1

Project description:Epigenetic profile of tissues is reprogrammed under diseased conditions. H3K4Me3 and H3K27Me3 represent active and repressive epigenetic marks, respectively. ChIP-seq is an effective tool to study global protein-DNA interactions. To study global epigenetic differences, we used H3K4Me3 antibody to evaluate its enrichment in pancreatic acinar cells of WT and Mist1-/- mice followed by next generation sequencing. We found specific hotspots that showed differential enrichment for H3K4Me3 both in WT and Mist1-/- mice. The data show that pancreatic acinar cells are epigenetically reprogrammed under stressed cellular conditions. Global H3K4Me3 profiling of WT and Mist1-/- pancreatic acinar cells using ChIP-seq.

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Project description:Aberrant acinar to ductal metaplasia (ADM), one of the earliest events involved in exocrine pancreatic cancer development, is typically studied using pancreata from transgenic mouse models. We used primary, human pancreatic acinar cells to evaluate the transcriptional profile during the course of ADM.

2022-06-01 | GSE179248 | GEO

Gene expression of non-apoptotic pancreatic acinar cell death with autophagy

Project description:Serine protease inhibitor Kazal type 3 (Spink3) is a trypsin inhibitor in the pancreas. Spink3-/- pancreatic acinar cells are dead with excessive autophagy at birth (p0.5). To prove the role of nonapoptotic cell death with autophagy, we generated by transgenic technology the pancreas of Spink3-/-;XKI/+ mice contained both normal and dying acinar cells with autophagy. In this new mouse model, chronic inflammation occurred in the pancreas, indicating that some signals from nonapoptotic dead cell induce chronic inflammation in the pancreas. All samples were the pancreas at p0.5. Sample 1 and 2 are the pancreas from wild type (Spink3+/+, control) mice. Sample 3 and 4 are the pancreas from Spink3-/-, which all pancreatic acinar cells show induced nonapoptotic cell death with autophagy. Sample 5 and 6 are the pancreas from Spink3-/-XKI/+, about half acinar cells are normal, but other acinar cells show induced nonapoptotic cell death with autophagy.

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