Loss of cytoskeletal support is not sufficient for anoxic plasma
membrane disruption in renal cells.
Chen, Jing, Jianwu Dai, Roberta L. Grant, R. Brian Doctor, Michael P.
Sheetz, and Lazaro J. Mandel.
DEPARTMENT OF CELL BIOLOGY, DUKE UNIVERSITY MEDICAL CENTER, DURHAM,
NC 27710
APStracts 3:0376C, 1996.
The goal of this study was to determine whether anoxic membrane
disruption is initiated by loss of cytoskeletal support in rabbit
renal proximal tubules (PT). We specifically tested: 1) whether
cytoskeletal perturbation affects membrane integrity under normoxia,
2) whether cytoskeletal perturbation potentiates anoxic membrane
damage, and 3) whether the membrane protection by glycine depends on
cytoskeletal integrity. Cytoskeletal perturbation was achieved using
10 [mu]M cytochalasin D (CD) because it selectively disturbs F-actin
organization and has similar effects as anoxia on the cytoskeleton of
PT. During normoxia, CD caused decreased basal F-actin content,
microvillar breakdown and membrane-cytoskeleton dissociation, as
revealed by the use of laser tweezers. However, membrane integrity
was not altered by CD, as monitored by lactate dehydrogenase release.
CD-pretreatment of PT did not potentiate anoxic membrane damage.
Finally, plasma membrane protection by glycine during anoxia remained
in CD-pretreated PT in spite of loss of cytoskeletal support. These
results demonstrate that loss of cytoskeletal support is not
sufficient for anoxic plasma membrane disruption.
Received 18 July 1996; accepted in final form 28 October 1996.
APS Manuscript Number C402-6.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996