Heat stress ameliorates atp depletion-induced sublethal injury in
mouse proximal tubule cells.
Borkan, S. C., Y. H. Wang, W. Lieberthal, P. R. Burke, and J. H.
Schwartz.
Renal Section, Evan's 428, Boston Medical Center, 88 East Newton
Street, Boston, MA 02118-2393
APStracts 3:0217F, 1996.
The role of prior heat stress (HS) in ameliorating changes in the
actin cytoskeleton and the loss of tight junction integrity that
accompany ATP depletion was examined. Mouse proximal tubule cells in
primary culture were exposed to CN in the absence of dextrose for 1
hr, a maneuver that produced equivalent degrees of ATP depletion in
control and in HS cells. Following ATP depletion, actin stress fibers
were completely disrupted in control cells. In contrast, HS cells
with elevated HSP 72 content showed preservation of stress fibers
after CN exposure. ATP depletion in control and HS cells produced
similar and reversible depletion of the G-actin pool without altering
total actin content. Integrity of the tight junction was assessed by
transepithelial electrical resistance (TER) and unidirectional flux
of lucifer yellow (LY, MW 482). After CN alone, the nadir in TER was
lower than that of HS + CN cells (51.6 2.5 vs. 96.2 3.2 .cm2,
respectively; P < 0.05). After 30 min recovery, TER of HS + CN
recovered to control values (277 7.2 vs. 227 6.6 .cm2; P > 0.05)
whereas CN did not (165 7.3 .cm2 vs. 227 6.6 .cm2; P < 0.05).
Changes in LY flux paralleled those in TER. HS is associated with
preservation of the actin cytoskeleton and improved integrity of the
tight junction after sublethal ATP depletion injury. These protective
effects may contribute to the preservation of epithelial cell
polarity and function following an ischemic insult.
Received 21 December 1995; accepted in final form 14 November
1996.
APS Manuscript Number F423-5.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996