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Vol. 10, Issue 4, 1247-1257, April 1999
Institute of Molecular Medicine and Genetics, Department of
Cellular Biology and Anatomy, Medical College of Georgia, Augusta, GA,
30912-2000.
Mechanically stressed cells display increased levels of fos message
and protein. Although the intracellular signaling pathways responsible
for FOS induction have been extensively characterized, we still
do not understand the nature of the primary cell mechanotransduction event responsible for converting an externally acting mechanical stressor into an intracellular signal cascade. We now report that plasma membrane disruption (PMD) is quantitatively correlated on a
cell-by-cell basis with fos protein levels expressed in mechanically injured monolayers. When the population of PMD-affected cells in
injured monolayers was selectively prevented from responding to the
injury, the fos response was completely ablated, demonstrating that PMD
is a requisite event. This PMD-dependent expression of fos protein did
not require cell exposure to cues inherent in release from cell-cell
contact inhibition or presented by denuded substratum, because it also
occurred in subconfluent monolayers. Fos expression also could not be
explained by factors released through PMD, because cell injury
conditioned medium failed to elicit fos expression. Translocation of
the transcription factor NF-
B into the nucleus may also be regulated
by PMD, based on a quantitative correlation similar to that found with
fos. We propose that PMD, by allowing a flux of normally impermeant
molecules across the plasma membrane, mediates a previously
unrecognized form of cell mechanotransduction. PMD may thereby lead to
cell growth or hypertrophy responses such as those that are present normally in mechanically stressed skeletal muscle and pathologically in
the cardiovascular system.
Corresponding author. E-mail address:
pmcneil{at}mail.mcg.edu.
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