{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"submitter":["Henrik Einwächter"],"organism":["Mus musculus"],"software":["Rupert Öllinger, PhD  Lab of Prof. Roland Rad  TranslaTUM Cancer Center, Institute of Molecular Oncology and Functional Genomics  Bau522/ 1.OG, R 1.25  Einsteinstr. 25 81675 München - Translatum, School of Medicine, Technical University of Munich"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-MTAB-15511"],"description":["Acute pancreatitis (AP) is defined by acute inflammatory injury to the pancreas and oxidative stress has been implicated as a mechanistic driver of disease progression. To delineate the contribution of reactive oxygen species (ROS) detoxification pathways in AP, we employed a genetic model of pancreas-specific deletion of the thioredoxin reductase 1 (Txnrd1) gene, either alone or in conjunction with pharmacological inhibition of glutathione synthesis via buthionine sulfoximine (BSO). AP was induced in these cohorts and in control animals. Pancreatic tissues were harvested at baseline (0 h), 8 h, 24 h, and 7 days post-induction for RNA sequencing to capture dynamic transcriptional programs. This experimental framework was designed to generate in vivo evidence on how modulation of ROS-scavenging systems influences pancreatic injury severity and subsequent repair processes in the context of AP."],"repository":["biostudies-arrayexpress"],"sample_protocol":["Nucleic Acid Extraction - Maxwell 16 Tissue LEV Total RNA Purification Kit was used for RNA extraction according to the manufacturer's instructions (Promega)","Library Construction - Library preparation for bulk 3’-sequencing of poly(A)-RNA was done as described previously (Parekh et al., 2016) barcoded cDNA of each sample was generated with a Maxima RT polymerase (Thermo Fisher) using oligo-dT primer containing barcodes, unique molecular identifiers (UMIs) and an adapter. 5’ ends of the cDNAs were extended by a template switch oligo (TSO) and after pooling of all samples full-length cDNA was amplified with primers binding to the TSO-site and the adapter. cDNA was tagmented with the Nextera XT kit (Illumina) and 3’-end-fragments finally amplified using primers with Illumina P5 and P7 overhangs.","Sequencing - The library was sequenced on a NextSeq 500 (Illumina) with 16 cycles for the barcodes and UMIs in read1 and 65 cycles for the cDNA in read2.","Sample Treatment - Acute pancreatitis was induced as published (Algül et al., JCI 2007), Buthionine sulphoximine (BSO) was given at 20mM in the drinking water  for 48 hours before AP induction","Sample Collection - Pancreatic tissue was collected from 8-12 week old mice"],"figure_sub":["Organization","MINSEQE Score","Assays and Data","Processed Data","MAGE-TAB Files"],"data_protocol":["Data Transformation - Data was processed using the published Drop-seq pipeline (v1.0) to generate sample- and gene-wise UMI tables (Macosko et al., 2015)."],"omics_type":["Unknown","Transcriptomics","Genomics","Proteomics"],"instrument_platform":["NextSeq 500"],"study_type":["RNA-seq of coding RNA"],"species":["Mus musculus"],"pubmed_authors":["Henrik Einwächter"],"additional_accession":[]},"is_claimable":false,"name":"Essential Role of Thioredoxin and Glutathione in Pancreas","description":"Acute pancreatitis (AP) is defined by acute inflammatory injury to the pancreas and oxidative stress has been implicated as a mechanistic driver of disease progression. To delineate the contribution of reactive oxygen species (ROS) detoxification pathways in AP, we employed a genetic model of pancreas-specific deletion of the thioredoxin reductase 1 (Txnrd1) gene, either alone or in conjunction with pharmacological inhibition of glutathione synthesis via buthionine sulfoximine (BSO). AP was induced in these cohorts and in control animals. Pancreatic tissues were harvested at baseline (0 h), 8 h, 24 h, and 7 days post-induction for RNA sequencing to capture dynamic transcriptional programs. This experimental framework was designed to generate in vivo evidence on how modulation of ROS-scavenging systems influences pancreatic injury severity and subsequent repair processes in the context of AP.","dates":{"release":"2025-08-30T00:00:00Z","modification":"2025-08-30T01:01:57.041Z","creation":"2025-08-22T14:40:07.841Z"},"accession":"E-MTAB-15511","cross_references":{"ENA":["ERP179038"],"EFO":["EFO_0002944","EFO_0004170","EFO_0005518","EFO_0003816","EFO_0003738","EFO_0004184","EFO_0003969"]}}