Mechanism of endothelial cell shape change in oxidant injury
dc.contributor.author | Hinshaw, Daniel B. | en_US |
dc.contributor.author | Burger, Jeanne M. | en_US |
dc.contributor.author | Armstrong, Barbara C. | en_US |
dc.contributor.author | Hyslop, Paul A. | en_US |
dc.date.accessioned | 2006-04-07T20:51:21Z | |
dc.date.available | 2006-04-07T20:51:21Z | |
dc.date.issued | 1989-04 | en_US |
dc.identifier.citation | Hinshaw, Daniel B., Burger, Jeanne M., Armstrong, Barbara C., Hyslop, Paul A. (1989/04)."Mechanism of endothelial cell shape change in oxidant injury." Journal of Surgical Research 46(4): 339-349. <http://hdl.handle.net/2027.42/27994> | en_US |
dc.identifier.uri | http://www.sciencedirect.com/science/article/B6WM6-4BNF621-3BP/2/57c821db4e89c618da40240ff239ef65 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/27994 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=2704230&dopt=citation | en_US |
dc.description.abstract | Changes in endothelial cell morphology induced by neutrophil-generated hydrogen peroxide (H2O2) may account for the capillary leak of the adult respiratory distress syndrome (ARDS). The relationship of H2O2 effects on the concentration of intracellular Ca2+([Ca2+]i) and ATP to changes in microfilaments and microtubules, important determinants of cell shape, was examined. Bovine pulmonary artery endothelial cells were injured over a 2-hr time course with a range of H2O2 doses (0-20 mM). The higher concentrations of H2O2 consistently produced contraction and rounding of>50-75% of cells by 1-2 hr. The range of 1-20 mM H2O2 produced rapid, significant reductions in endothelial ATP levels over the time course of injury. Although there were significant increases in mean endothelial [Ca2+]i in response to 5, 10, and 20 mM H2O2, 1 mMH2O2 did not affect the [Ca2+]i. Fluorescence microscopy revealed that microfilament disruption occurred as ATP levels fell and preceded depolymerization of microtubules which developed after [Ca2+]1 approached 1 x 10-6 M. H2O2 at 1 mM injury caused microfilament disruption but did not depolymerize microtubules. Microfilament disruption occurred without oxidant exposure, when ATP levels were reduced by glucose depletion and mitochondrial inhibition with oligomycin (650 nM). If a Ca2+ ionophore, ionomycin (5 [mu]M), was then added, [Ca2+]i rose to > 1 x 10-6 M, microtubules fragmented and depolymerized, and cell contraction and rounding very similar to that induced by H2O2 occurred. These results suggest that endothelial cell dysfunction and capillary leak in ARDS may be due to H2O2-mediated changes in cellular ATP and [Ca2+]i. | en_US |
dc.format.extent | 1178207 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Elsevier | en_US |
dc.title | Mechanism of endothelial cell shape change in oxidant injury | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Surgery and Anesthesiology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Surgery, University of Michigan, and Ann Arbor VA Medical Center, Ann Arbor, Michigan 48105, USA | en_US |
dc.contributor.affiliationum | Department of Surgery, University of Michigan, and Ann Arbor VA Medical Center, Ann Arbor, Michigan 48105, USA | en_US |
dc.contributor.affiliationother | McGuire VA Medical Center, Richmond, Virginia, USA | en_US |
dc.contributor.affiliationother | Lilly Research Laboratories, Indianapolis, Indiana, USA | en_US |
dc.identifier.pmid | 2704230 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/27994/1/0000428.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1016/0022-4804(89)90199-6 | en_US |
dc.identifier.source | Journal of Surgical Research | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
Files in this item
Remediation of Harmful Language
The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.
Accessibility
If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.