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Influence of protein kinase C on transcription of the tight junction elements ZO‐1 and occludin
Author(s) -
Weiler Frank,
Marbe Theresa,
Scheppach Wolfgang,
Schauber Jürgen
Publication year - 2005
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.20268
Subject(s) - occludin , protein kinase c , tight junction , microbiology and biotechnology , transcription factor , paracellular transport , signal transduction , mapk/erk pathway , chemistry , biology , biochemistry , gene , membrane , permeability (electromagnetism)
Tight junctions as an epithelial barrier against paracellular diffusion have mainly been investigated on the protein level with particular respect to subcellular localization. In this study, real‐time PCR has been established to investigate the influence of protein kinase C (PKC) modulation on the transcription of tight junction elements occludin and ZO‐1 in the cell line T84. Activation of PKC by the phorbol ester TPA induced ZO‐1 and occludin transcription, whereas PKC inhibition lead to decreased expression levels. Activation of PKC exerted its effect on transcript level directly. PKC signal was partially transduced via MEK1/MEK2 but depended strongly on MAPK independent pathways probably involving nuclear localized PKC, whereas p38 signaling was not implicated. TPA induced loss of function concomitant with a dislocation of ZO‐1 and occludin could be prevented by inhibition of MEK1 by PD98059. Overall ZO‐1 and occludin seem to be identically regulated in colonic epithelium on the transcript level. © 2004 Wiley‐Liss, Inc.