Tight junctions in human pancreatic duct epithelial cells

Abstract

Tight junctions of the pancreatic duct are essential regulators of physiologic secretion of the pancreas and disruption of the pancreatic ductal barrier is known to contribute to the pathogenesis of pancreatitis and progression of pancreatic cancer. Various inflammatory mediators and carcinogens can trigger tight junction disassembly and disruption of the pancreatic barrier, however signaling events that mediates such barrier dysfunctions remain poorly understood. This review focuses on structure and regulation of tight junctions in normal pancreatic epithelial cells and mechanisms of junctional disruption during pancreatic inflammation and cancer. We will pay special attention to a novel model of human telomerase reverse transcriptase-transfected human pancreatic ductal epithelial cells and will describe the roles of major signaling molecules such as protein kinase C and c-Jun N-terminal kinase in formation and disassembly of the pancreatic ductal barrier.

Keywords: :

• tight junctions
• normal human pancreatic duct epithelial cells
• pancreatic cancer
• PKC
• JNK

Submitted

01/17/2013

Revised

04/28/2013

Accepted

05/01/2013

Disclosure of Potential Conflicts of Interest

The authors declare no conflicts of interest.

Acknowledgments

This work was supported by the Pancreas Research Foundation of Japan and the Ministry of Education, Culture, Sports, Science and Technology and the Ministry of Health, Labour and Welfare of Japan.