Project description:There still is a lack of specific, early markers for acute pancreatitis. We used the gene expression profiling Affimetrix mouse gene 1.0 ST arrays (Affymetrix , Inc. Santa Clara, CA), to cmpare the gene expression between control mice and mice with induced experimental acute pancreatitis, in order to identify new potential biomarkers of acute pancreatitis.
Project description:A frequently used experimental model of chronic pancreatitis (PC) recapitulating human disease is repeated injection of cerulein to mice. We found that two common substrains of C57BL/6 , C56BL/6J (Jackson) and C57BL/6NHsd (Harlan), exhibit different degree of CP with C57BL/6J beeing more susceptible to repetitive cerulein induced CP. The goal of this study was to identify genes associated with CP and also to identify genes differentially regulated between two substrains as candidates for the CP progression. RNAs were isolated from the pancreas of 8-week old Jackson and Harlan mice after the cerulein induction of chronic pancreatitis and hybridized on Affymetrix microarrays. Saline injected mice were used as controls. Three mice from each experimental and control groups were used in the experiment.
Project description:A frequently used experimental model of chronic pancreatitis (PC) recapitulating human disease is repeated injection of cerulein to mice. We found that two common substrains of C57BL/6 , C56BL/6J (Jackson) and C57BL/6NHsd (Harlan), exhibit different degree of CP with C57BL/6J beeing more susceptible to repetitive cerulein induced CP. The goal of this study was to identify genes associated with CP and also to identify genes differentially regulated between two substrains as candidates for the CP progression.
Project description:We have studied pancreas samples in pancreas from a mouse model of acute pancreatitis, comparing wild-type animals and TRP14 KO animals. Samples are extracted with N-ethylmaleimide to block reduced cysteines, and no reducing agent is used, with a search including cysteinylated peptides. Acute pancreatitis was induced in 12 weeks-old mice (wild-type and KO for TRP14) by seven intraperitoneal injections of cerulein (50 µg/kg body weight) at 1 h intervals. Then, 1 h after the last injection, animals were euthanized under anesthesia with 3% isoflurane, exsanguinated, and the pancreas was immediately removed and processed.
Project description:mRNA was isolated from duodenal tissue 3d after induction of acute pancreatitis in C57Bl/6 wild type mice to investigate transcriptional changes, untreated C57Bl/6 refer as controls we used microarrays to investigate the duodenal barrier function during acute pancreatitis
Project description:Pancreas tissue derived from mice with intraperitoneal injection of saline, cerulein or polyI:C plus cerulein, total RNA was extracted and deep sequenced to compare the gene expression profiles among control, acute pancreatitis and intervention of polyI:C on acute pancreatitis.
Project description:Transgenic KrasG12D mice can recapitulate pancreas intra-epithelial neoplasia (PanIN). Caerulein is a cholecystokinin analogue and induces acute pancreatitis when injected intra-abdominally. Caerulein-induced acute pancreatitis will accelerate PanIN progression in KrasG12D mice. We compared mRNA profile changes between KrasG12D mice with acute caerulein-induced pancreatitis and wild-type mice without acute pancreatitis. The experiment had two groups. Experiment group: KrasG12D mice with acute caerulein-induced pancreatitis (N=6). Three mice in experiment group received 1-week caerulein injection, and the other three mice received 2-week caerulein injection. All experiment group mice started to receive caerulein injection at 1-month of age, and were sacrificed at the last day of caerulein injection. Control group: wild-type mice without acute pancreatitis (N=6). The mice were sacrificed at 1.5-month of age. Whole pancreas tissue lysate samples were subjected to mRNA array assay.
Project description:To determine the molecular basis of gene regulation in pancreatic ductal epithelial cells, we developed methods for the isolation of this cell population during mouse development and normal adult homeostasis, as well as in conditions with ductal features (acinar-to-ductal metaplasia (ADM), pancreatic intraepithelial neoplasia (PanIN) and pancreatic ductal adenocarcinoma (PDAC)). Our technique utilizes the specificity of Dolichos biflorus Agglutinin (DBA) lectin marking the entire normal ductal tree, including terminal intercalated ducts (putative sites of stem or progenitor cells) and ductal structures in ADM and PanIN. We used ferromagnetic-labeled DBA lectin to isolate ductal structures. Ductal cells were isolated under the following conditions: (1) Embryonic Development in wild type mice: E14.5, E15.5, E16.5, and postnatal day 1 (P1); (2) Injury and regeneration (pancreatitis) 0, 1, 3, 5 days following cerulein-induced acute pancreatitis. Cerulein is a cholecystokinin analog which produces a self-limited pancreatitis with injury and subsequent regeneration and repair, completed five days after insult; and (3) Pdx1-Cre;LSL-KrasG12D/+ mice aged 10 and 20 weeks that harbor PanIN lesions and a subset develop PDAC. Ductal/PanIN cells were isolated from these mice and appropriate control mice (Pdx1-Cre;Kras+/+).
Project description:Based on the role of lactate in mitigating inflammation during acute pancreatitis (AP) repair, we focused on macrophages, as previous studies have highlighted their essential role in pancreatic tissue repair following AP. To investigate the relationship between lactate and the phenotype and function of macrophages during the recovery phase after AP, we performed high-throughput mRNA sequencing on macrophages isolated from the pancreatic tissues of C57BL/6J wild-type mice, which were administered lactate or PBS following induction of a recovery AP model.
Project description:Transgenic KrasG12D mice can recapitulate pancreas intra-epithelial neoplasia (PanIN). Caerulein is a cholecystokinin analogue and induces acute pancreatitis when injected intra-abdominally. Caerulein-induced acute pancreatitis will accelerate PanIN progression in KrasG12D mice. We compared mRNA profile changes between KrasG12D mice with acute caerulein-induced pancreatitis and wild-type mice without acute pancreatitis.