Am J Physiol Cell Physiol Track the topics, authors and articles important to you
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol 272: C1319-C1328, 1997;
0363-6143/97 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Chen, J.
Right arrow Articles by Mandel, L. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chen, J.
Right arrow Articles by Mandel, L. J.

AJP - Cell Physiology, Vol 272, Issue 4 C1319-C1328, Copyright © 1997 by American Physiological Society

ARTICLES

Loss of cytoskeletal support is not sufficient for anoxic plasma membrane disruption in renal cells

J. Chen, J. Dai, R. L. Grant, R. B. Doctor, M. P. Sheetz and L. J. Mandel
Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.

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 with 10 microM 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 despite loss of cytoskeletal support. These results demonstrate that loss of cytoskeletal support is not sufficient for anoxic plasma membrane disruption.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Renal Physiol.Home page
F. A. Wald, Y. Figueroa, A. S. Oriolo, and P. J. I. Salas
Membrane repolarization is delayed in proximal tubules after ischemia-reperfusion: possible role of microtubule-organizing centers
Am J Physiol Renal Physiol, August 1, 2003; 285(2): F230 - F240.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
J. Chen and M. C. Wagner
Altered membrane-cytoskeleton linkage and membrane blebbing in energy-depleted renal proximal tubular cells
Am J Physiol Renal Physiol, April 1, 2001; 280(4): F619 - F627.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
P. White, R. B. Doctor, R. H. Dahl, and J. Chen
Coincident microvillar actin bundle disruption and perinuclear actin sequestration in anoxic proximal tubule
Am J Physiol Renal Physiol, June 1, 2000; 278(6): F886 - F893.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
J. Chen and L. J. Mandel
Role of water and electrolyte influxes in anoxic plasma membrane disruption
Am J Physiol Cell Physiol, October 1, 1997; 273(4): C1341 - C1348.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online