Project description:Total pancreatectomy with islet cell autotransplantation (TPIAT) is a surgical treatment modality used for the management of painful chronic pancreatitis when medical and endoscopic therapies fail. Total pancreatectomy (TP) results in a number of clinical implications. However, the glucose-responsive insulin secretion can be preserved by combining TP with islet cell autotransplant (IAT). Despite the known clinical implications of TPIAT, the systemic molecular effects of TPIAT remains poorly investigated. Therefore, we performed the first hypothesis-generating study of the urinary proteome before and after TPIAT. The RAW- and processed data from the analysis can be found in this repository. Twenty-two chronic pancreatitis patients eligible for TPIAT were prospectively enrolled in the study at the University of Minnesota Medical Center between September 2011 and February 2014. Urine was collected within the week pre-TPIAT and 12-18 months post-TPIAT, resulting in 44 paired samples. The paired experimental design allowed us to subtract interpersonal differences. The unique set of urine samples were prepared for bottom-up label-free quantitative proteomics using the in-house developed ‘MStern’ protocol for the 96-well plate compatible processing of the urine samples. The samples were analyzed by LC-MS/MS and 2477 proteins were identified (FDR<0.01%). Five samples were found to have less than 30% of the cumulated list of proteins (<743 proteins) and so these samples and their respective matching sample were thus removed from the analysis. This resulted in a complete dataset with 17 matched pre- and post-TPIAT sample pairs. The final list of recommended included pairs for future analysis are indicated in the PX_TPIAT_Metadata.csv file. Note that extended clinical information only was available for the included samples. Furthermore, the information is only listed for the pre-TPIAT sample but applies to both the pre- and post-TPIAT participant sample. The data allows for studying the systemic molecular impact of the TPIAT procedure.
Project description:To determine how ARID1A loss might regulate gene expression, we performed RNA-sequencing (RNA-seq) on islets isolated from control and Arid1a knockout (KO) mice at baseline and 6 days after 50% pancreatectomy (PPx).
Project description:To determine how ARID1A loss might regulate gene expression, we performed RNA-sequencing (RNA-seq) on islets isolated from control and Arid1a knockout (KO) mice at baseline and 6 days after 50% pancreatectomy (PPx).
Project description:Diabetes mellitus results from an inadequately functioning beta-cell mass. In the adult pancreas, beta-cell mass is dynamic, increasing to meet metabolic demands and decreasing with metabolic or injury insults. Exendin-4 (Ex-4) is a glucagon-like peptide-1 receptor agonist that augments beta-cell mass by increasing beta-cell neogenesis and proliferation and by reducing apoptosis. We utilized a cDNA microarray approach to identify genes that are differentially regulated during islet growth after Ex-4 treatment or a partial pancreatectomy (Ppx). Mice underwent 50% Ppx or sham operation and received Ex-4 or vehicle every 24 hours. cDNA prepared from total pancreatic RNA isolated at 12, 24 and 48 hrs after surgery was hybridized to the PancChip 4.0 microarray.
Project description:We employed single-cell RNA sequencing of islets in young mice subjected to partial pancreatectomy (PPTx). Four clusters of pancreatic beta cells including a subpopulation of replicating beta cells. Pseudo-time course analysis clarified the gradual changes in gene expression from non-replicating beta cells to replicating ones. Upstream analysis visualized the transcriptional networks associated with beta cell replication by PPTx.
