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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
	SRR13199700.fastq.gz	Fastqsanger.gz
	SRR13199701.fastq.gz	Fastqsanger.gz
	SRR13199702.fastq.gz	Fastqsanger.gz
	SRR13199703.fastq.gz	Fastqsanger.gz
	SRR13199704.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.

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

Project description:Despite 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. The 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. We 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. Taken 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.

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