https://www.journal-of-hepatology.eu/article/S0168-8278(15)00249-4/pdf

Hepatic cell proliferation plays a pivotal role in the prognosis of alcoholic hepatitis.

The present study aimed to identify the differential expressed genes that are related to acute pancreatitis. Microarray datasets GSE109227 and GSE3644 were downloaded from the public database and analyzed to screen the genes. Afterward, integrated analysis of these genes were performed, including gene ontology and pathway enrichment analysis, protein–protein interaction network construction, expression level evaluation in human organs, relevant miRNAs and TFs prediction, and prognosis values of hub genes in pancreatic carcinoma. A total number of 93 differential expressed genes were screened from the datasets, and EGFR, CDH1, ACTB, CD44, and VCL were identified as hub DEGs. Functional enrichment analysis demonstrated that these genes were mostly enriched in biological processes such as cell adhesion, platelet aggregation, glycoprotein binding, and also involved in multiple pathways included adherent junction, proteoglycans in cancer, bacterial invasion of epithelial cells, focal adhesion, Rap1 signaling pathway, regulation of actin cytoskeleton, and pathways in cancers. The five hub genes were all expressed in human pancreas organs with various levels. Hub gene-related network investigation predicted core miRNAs including hsa-mir-16-5p and main TFs like SOX9 with close interactions with these hub genes. Survival analysis also indicated that the high expression of EGFR, CDH1, ACTB, CD44, and VCL were significantly associated with poor prognosis in pancreatic carcinoma. The study suggested that hub genes EGFR, CDH1, ACTB, CD44, and VCL may play vital role in the pathogenesis of acute pancreatitis and may serve as potential biomarkers to facilitate future acute pancreatitis diagnosis and treatment.

Identification of Acute Pancreatitis-Related Genes and Pathways by Integrated Bioinformatics Analysis

Autophagy regulation in pancreatic acinar cells is independent of epidermal growth factor receptor signaling.

Double deficiency of cathepsin B and L in the mouse pancreas alters trypsin activity without affecting acute pancreatitis severity.

Serine peptidase inhibitor, Kazal type 3 (SPINK3) is a trypsin inhibitor, and also a growth factor that has an identical structure to epidermal growth factor (EGF), which could combine with epidermal growth factor receptor (EGFR) to promote cell proliferation. To shed light on the role and regulation mechanism of SPINK3 in rat liver regeneration (LR), Rat Genome 230 2.0 assay was used to detect the expression profiles of LR genes after partial hepatectomy (PH). The results showed that Spink3 was significantly up-regulated at 2-24 h and 72-168 h after PH. In the present study, RT-PCR and immunoblotting were used to validate the assay results. Ingenuity Pathway Analysis 9.0 (IPA) software was used to build the SPINK3 signaling regulating LR and analyze the possible mechanism. And then the expression of cell proliferation-associated gene Ccna2 was examined by RT-PCR in normal rat liver cell line BRL-3A in which Spink3 was overexpressed. The results showed that Ccna2 was significantly up-regulated in BRL-3A in which Spink3 was over-expressed. SPINK3 combining with EGFR accelerated cell proliferation during rat liver regeneration via P38, PKC, JAK-STAT and AKT pathways. Thus, SPINK3 was likely to promote hepatocytes proliferation in LR through P38, PKC, JAK-STAT and AKT.

SPINK3: A novel growth factor that promotes rat liver regeneration

Serine protease inhibitor Kazal type 1 (SPINK1; mouse homologue Spink3) was initially discovered as a trypsin-specific inhibitor in the pancreas. However, previous studies have suggested that SPINK1/Spink3 is expressed in a wide range of normal tissues and tumors, although precise characterization of its gene expression has not been described in adulthood. To further analyze Spink3 expression, we generated two mouse lines in which either lacZ or Cre recombinase genes were inserted into the Spink3 locus by Cre-loxP technology. In Spink3 lacZ mice, β-galactosidase activity was found in acinar cells of the pancreas and kidney, as well as epithelial cells of the bronchus in the lung, but not in the gastrointestinal tract or liver. Spink3 cre knock-in mice were crossed with Rosa26 reporter (R26R) mice to monitor Spink3 promoter activity. In Spink3 cre ;R26R mice, β-galactosidase activity was found in acinar cells of the pancreas, kidney, lung, and a small proportion of cells in the gastrointestinal tract and liver. These data suggest that Spink3 is widely expressed in endoderm- derived tissues, and that Spink3 cre knock-in mice are a useful tool for establishment of a conditional knockout mice to analyze Spink3 function not only in normal tissues, but also in tumors that express

Generation and Analysis of Serine Protease Inhibitor Kazal Type 3-Cre Driver Mice

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Generation and Analysis of Serine Protease Inhibitor Kazal Type 3-Cre Driver Mice

Autophagy regulation in pancreatic acinar cells is independent of epidermal growth factor receptor signaling.