Cell surface repair PNAS

Cell surface repair PNAS - The endomembrane requirement for...

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The endomembrane requirement for cell surface repair Paul L. McNeil* , Katsuya Miyake*, and Steven S. Vogel ‡§ *Department of Cellular Biology and Anatomy, and Department of Medicine and Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, GA 30912 Edited by Kai Simons, Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany, and approved February 11, 2003 (received for review December 2, 2002) The capacity to reseal a plasma membrane disruption rapidly is required for cell survival in many physiological environments. Intracellular membrane (endomembrane) is thought to play a central role in the rapid resealing response. We here directly compare the resealing response of a cell that lacks endomembrane, the red blood cell, with that of several nucleated cells possessing an abundant endomembrane compartment. RBC membrane dis- ruptions inFicted by a mode-locked Ti:sapphire laser, even those initially smaller than hemoglobin, failed to reseal rapidly. By contrast, much larger laser-induced disruptions made in sea urchin eggs, ±broblasts, and neurons exhibited rapid, Ca 2 1 -dependent resealing. We conclude that rapid resealing is not mediated by simple physiochemical mechanisms; endomembrane is required. P lasma membrane disruption, induced by physiologically gen- erated mechanical stress, is a common form of cell injury in many mammalian tissues (1). Potentially, this could result in significant loss of nonrenewing cell types, such as neurons and cardiac myocytes, or large cells that are especially prone to disruption injury, such as skeletal muscle cells. That such loss does not occur in vivo can be explained by the widespread capacity of animal cells for rapid resealing of plasma membrane disruptions. Perhaps paradoxically, given its toxic properties (2), Ca 2 1 , present at physiological levels in the external environment, is required for nucleated animal cell resealing of disruptions ranging from 1 to 1000 m m 2 in extent (3). The principal function proposed for this extracellular Ca 2 1 is as signal-triggering ho- motypic and heterotypic membrane fusion responses. Thus, Ca 2 1 -dependent exocytotic (cytoplasmic vesicle–plasma mem- brane) and homotypic (vesicle–vesicle) fusion events have clearly been demonstrated to correlate spatially, temporally, and quantitatively with the resealing response in fibroblasts and eggs (4–6). If these cytoplasmic membrane-dependent fusion events are required for, and are not simply correlates of, rapid resealing, then a simple prediction follows: a cell lacking cytoplasmic membrane (endomembrane) will be incapable of rapid resealing. The mammalian RBC, because it lacks endomembrane, provides an opportunity to test this prediction directly. Although RBC resealing (recovery of near-normal perme- ability characteristics) after osmotic lysis (7) and electroporation (8) has been characterized, the RBC resealing response has never been compared directly in physiological calcium with that of nucleated cells wounded by identical means. Moreover,
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Cell surface repair PNAS - The endomembrane requirement for...

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