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

Jing Chen, Jianwu Dai, Roberta L. Grant, R. Brian Doctor, Michael Sheetz, Lazaro J. Mandel

Research output: Contribution to journalArticle

15 Scopus citations


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 μM 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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Cell Physiology
Issue number4 41-4
StatePublished - May 21 1997
Externally publishedYes



  • cytochalasin D
  • glycine
  • lactate dehydrogenase release
  • laser tweezers
  • membrane integrity

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

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