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lüll Expression of interleukin-24 and its receptor in human pancreatic myofibroblasts Imaeda H; Nishida A; Inatomi O; Fujiyama Y; Andoh AInt J Mol Med 2011[Dec]; 28 (6): 993-9Interleukin (IL)-24 is a member of the IL-10 family of cytokines. In this study, we investigated IL-24 expression in chronic pancreatitis tissue and characterized the molecular mechanisms responsible for IL-24 expression in human pancreatic myofibroblasts. IL-24 expression in the tissues was evaluated by immunohistochemical methods. IL-24 mRNA and protein expression in the pancreatic myofibroblasts was determined by real-time-PCR and ELISA, respectively. IL-24 was expressed by alpha-smooth muscle actin-positive myofibroblasts in the chronic pancreatitis tissues. In isolated human pancreatic myofibroblasts, IL-1beta significantly enhanced IL-24 mRNA and protein expression. The p38 MAPK inhibitor SB203580 and the PI3K inhibitor LY294002 significantly reduced the IL-beta-induced IL-24 mRNA expression. An adenovirus containing a dominant-negative mutant of c-Jun significantly inhibited the effects of IL-1beta on IL-24 mRNA expression, indicating that the IL-1beta-induced IL-24 mRNA expression was mediated by the activation of transcription factor AP-1. Pancreatic myofibroblasts expressed IL-22R1, IL-20R1 and IL-20R2, and recombinant IL-24 induced the phosphorylation of p42/44, p38, JNK and STAT1/3. IL-24 is expressed in chronic pancreatitis tissue, and may play a role in the pathophysiology of chronic pancreatitis via autocrine pathways.|Enzyme-Linked Immunosorbent Assay[MESH]|Gene Expression/drug effects[MESH]|Humans[MESH]|Interleukin-1beta/*pharmacology[MESH]|Interleukins/genetics/*metabolism[MESH]|Mitogen-Activated Protein Kinase 1/genetics/metabolism[MESH]|Mitogen-Activated Protein Kinase 3/genetics/metabolism[MESH]|Myofibroblasts/cytology/*metabolism[MESH]|Pancreatitis, Chronic/genetics/*metabolism/pathology/*physiopathology[MESH]|Phosphatidylinositol 3-Kinases/genetics/metabolism[MESH]|Phosphoinositide-3 Kinase Inhibitors[MESH]|Phosphorylation/drug effects[MESH]|Primary Cell Culture[MESH]|Protein Kinase Inhibitors/*pharmacology[MESH]|RNA, Messenger/biosynthesis[MESH]|Real-Time Polymerase Chain Reaction[MESH]|Receptors, Interleukin/genetics/*metabolism[MESH]|Signal Transduction/drug effects[MESH]|Transcription Factor AP-1/genetics/metabolism[MESH]|p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/genetics/metabolism[MESH] |