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1 increases MLC phosphorylation
and endothelial monolayer permeability
Center for Cardiovascular Sciences, Albany Medical College, Albany, New York 12208
Transforming growth
factor (TGF)-
1 increases endothelial monolayer permeability and
myosin light chain phosphorylation (MLC-P) beginning 1-2 h
posttreatment, suggesting that changes in gene expression may be
required for these responses. The role of extracellular signal-regulated kinase (ERK) 1/2 and p38 mitogen-activated protein kinase (p38 MAPK) was investigated because both kinases have been implicated in regulating gene expression after TGF-1. ERK1/2 phosphorylation increased threefold above the control level, and the
increase was temporally associated with the increase in MLC-P. Inhibition of ERK1/2 phosphorylation with the MAPK kinase inhibitor U-0126 did not prevent the increase in either monolayer permeability or
MLC-P. p38 MAPK phosphorylation increased fourfold above the control
level, but unlike ERK1/2, this increase peaked 30 min and 1 h
post-TGF-1 treatment. Inhibition of p38 MAPK activity with SB-203580
prevented the increases in both monolayer permeability and MLC-P.
Treatment of the monolayers with cycloheximide in conjunction with
TGF-1-inhibited MLC-P, showing a requirement for protein synthesis.
These studies demonstrate that p38 MAPK activation and subsequent
protein synthesis are part of the signal transduction pathway leading
to the TGF-1-induced increases in monolayer permeability and
MLC-P.
transforming growth factor-1; myosin light chain
phosphorylation; endothelial cells; cycloheximide; mitogen-activated
protein kinase
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