NDLI: Inhibition of Src and p38 MAP kinases suppresses the change of claudin expression induced on dedifferentiation of primary cultured parotid acinar cells.

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Inhibition of Src and p38 MAP kinases suppresses the change of claudin expression induced on dedifferentiation of primary cultured parotid acinar cells.

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Inhibition of Src and p38 MAP kinases suppresses the change of claudin expression induced on dedifferentiation of primary cultured parotid acinar cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Fujita-Yoshigaki, Junko Matsuki-Fukushima, Miwako Sugiya, Hiroshi
Description	Country affiliation: Japan Author Affiliation: Fujita-Yoshigaki J ( Dept. of Physiology, Nihon Univ. School of Dentistry at Matsudo, Sakaecho-nishi 2-870-1, Matsudo, Chiba 271-8587, Japan. yoshigaki.junko@nihon-u.ac.jp)
Abstract	Sjögren's syndrome and therapeutic radiation for head and neck cancers result in irreversible changes in the parenchyma of salivary glands, loss of acinar cells, prominence of duct cells, and fibrosis. To clarify mechanisms of salivary gland dysfunction, we identified a signaling pathway involved in the dedifferentiation of primary cultures of parotid acinar cells. We reported previously that the expression pattern of claudins changes during culture, is related to the three-dimensional organization of the cells, and reflects their ability to function as acinar cells. In this study, we found that this change of claudin expression is a process of dedifferentiation, because expression of other differentiation markers also changes during culture. The expression levels of claudins-4 and -6, cytokeratin 14, and vimentin are increased, and those of claudin-10, aquaporin 5, and amylase are decreased. Inhibitors of Src and p38 MAP kinases suppress these changes and increase the expression of acinar marker proteins. Differences in extracellular matrix components have no effect. Activation of p38 MAP kinase occurs during cell isolation from the parotid glands and is retained up to 6 h after the isolation. In contrast, activation of Src kinases does not increase during the cell isolation. The Src inhibitor PP1 suppresses the activation of p38 MAP kinase. Therefore, cellular stresses induced during cell isolation cause dedifferentiation and transition to duct-like cells through activation of p38 MAP kinase and constitutively active Src kinases.
File Format	HTM / HTML
ISSN	03636143
e-ISSN	15221563
Journal	American Journal of Physiology - Cell Physiology
Issue Number	3
Volume Number	294
Language	English
Publisher	American Physiological Society
Publisher Date	2008-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Cell Differentiation Drug Effects Membrane Proteins Metabolism Parotid Gland Protein Kinase Inhibitors Pharmacology Signal Transduction P38 Mitogen-activated Protein Kinases Antagonists & Inhibitors Src-family Kinases Amylases Animals Anthracenes Aquaporin 5 Butadienes Cell Adhesion Cell Culture Techniques Cell Proliferation Cell Shape Cells, Cultured Claudin-4 Claudins Enzyme Activation Extracellular Matrix Imidazoles Keratin-14 Nitriles Cytology Enzymology Pyrazoles Pyridines Pyrimidines Rats, Sprague-dawley Tight Junctions Time Factors Vimentin Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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