Role of Janus Kinase/Signal Transducers and Activators of Transcription in the Pathogenesis of Pancreatitis and Pancreatic Cancer.
- Author:
Ji Hoon YU
1
;
Hyeyoung KIM
Author Information
1. Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
- Publication Type:Original Article
- Keywords:
JAK/STAT;
Pancreatitis;
Pancreatic cancer;
Oxidative stress
- MeSH:
Acinar Cells;
Apoptosis;
Caerulein;
Cell Proliferation;
Cholecystokinin;
Cytokines;
Humans;
Interleukin-6;
Interleukins;
NADP;
Oxidative Stress;
Oxidoreductases;
Pancreas;
Pancreatic Neoplasms;
Pancreatitis;
Phosphorylation;
Reactive Oxygen Species;
Rodentia;
STAT3 Transcription Factor;
Transducers;
Tumor Necrosis Factor-alpha
- From:Gut and Liver
2012;6(4):417-422
- CountryRepublic of Korea
- Language:English
-
Abstract:
In the pathogenesis of pancreatitis, oxidative stress is involved in the activation of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway and cytokine expression. High serum levels of cholecystokinin (CCK) have been reported in patients with acute pancreatitis, and treatment with cerulein, a CCK analogue, induces acute pancreatitis in a rodent model. Recent studies have shown that cerulein-activated nicotinamide adenine dinucleotide phosphate oxidase elicits reactive oxygen species, which trigger the phosphorylation of the JAK1, STAT1, and STAT3 proteins and induce the production of inflammatory cytokines, such as tumor necrosis factor-alpha, interleukin (IL)-1beta, and IL-6, in pancreatic acinar cells. The JAK/STAT pathway also stimulates cell proliferation and malignant transformation and inhibits apoptosis in the pancreas. This review discusses the possible role of the JAK/STAT pathway in the pathogenesis of pancreatitis and pancreatic cancer in response to oxidative stress.
