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Conference Paper: Response of the human peritoneal mesothelial cell to injury: An in vitro model of peritoneal wound healing

TitleResponse of the human peritoneal mesothelial cell to injury: An in vitro model of peritoneal wound healing
Authors
Issue Date1998
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.html
Citation
Kidney International, 1998, v. 54 n. 6, p. 2160-2169 How to Cite?
AbstractBackground. The denudation of the peritoneal mesothelium and damage to the underlying interstitium is a frequent finding in patients receiving continuous ambulatory peritoneal dialysis as a treatment for end-stage renal failure. The response of the mesothelium to injury from repeated episodes of infection or from exposure to dialysis fluids has not been extensively studied. The present study describes a simple and reproducible method with which to investigate the response of human mesothelial cells to injury. Methods. The model of peritoneal injury consists of mechanically wounding a monolayer of human peritoneal mesothelial cells with a glass probe and following the repopulation of the denuded area by time-lapse photomicroscopy. In addition immunohistochemistry was used to follow the response of marker proteins for stress fibers and focal adhesions as well as macromolecules associated with the extracellular matrix. Results. Under serum-free conditions the wound (0.58 ± 0.094 mm; mean ± SD; N = 20) closed within 72 ± 5 hours (N = 8). This rate of healing was enhanced by fetal calf serum, by human serum (10%) and by undiluted spent non-infected dialysate. The repair process over the first 48 hours was the result of cell migration, was independent of cell proliferation and involved the de novo synthesis of several different extracellular matrix components. An early event in the healing process was the rapid reorganization of intracellular stress fibers together with the formation of associated focal adhesions in cells at the wound edge. Conclusion. This in vitro model should prove invaluable in characterizing the process of wound healing within the peritoneal cavity, thus allowing a better understanding of the response to infection as well as any effect of dialysis fluids in this pattern of cell behavior.
Persistent Identifierhttp://hdl.handle.net/10722/163546
ISSN
2015 Impact Factor: 7.683
2015 SCImago Journal Rankings: 3.181
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYung, Sen_US
dc.contributor.authorDavies, Men_US
dc.date.accessioned2012-09-05T05:37:18Z-
dc.date.available2012-09-05T05:37:18Z-
dc.date.issued1998en_US
dc.identifier.citationKidney International, 1998, v. 54 n. 6, p. 2160-2169en_US
dc.identifier.issn0085-2538en_US
dc.identifier.urihttp://hdl.handle.net/10722/163546-
dc.description.abstractBackground. The denudation of the peritoneal mesothelium and damage to the underlying interstitium is a frequent finding in patients receiving continuous ambulatory peritoneal dialysis as a treatment for end-stage renal failure. The response of the mesothelium to injury from repeated episodes of infection or from exposure to dialysis fluids has not been extensively studied. The present study describes a simple and reproducible method with which to investigate the response of human mesothelial cells to injury. Methods. The model of peritoneal injury consists of mechanically wounding a monolayer of human peritoneal mesothelial cells with a glass probe and following the repopulation of the denuded area by time-lapse photomicroscopy. In addition immunohistochemistry was used to follow the response of marker proteins for stress fibers and focal adhesions as well as macromolecules associated with the extracellular matrix. Results. Under serum-free conditions the wound (0.58 ± 0.094 mm; mean ± SD; N = 20) closed within 72 ± 5 hours (N = 8). This rate of healing was enhanced by fetal calf serum, by human serum (10%) and by undiluted spent non-infected dialysate. The repair process over the first 48 hours was the result of cell migration, was independent of cell proliferation and involved the de novo synthesis of several different extracellular matrix components. An early event in the healing process was the rapid reorganization of intracellular stress fibers together with the formation of associated focal adhesions in cells at the wound edge. Conclusion. This in vitro model should prove invaluable in characterizing the process of wound healing within the peritoneal cavity, thus allowing a better understanding of the response to infection as well as any effect of dialysis fluids in this pattern of cell behavior.en_US
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.htmlen_US
dc.relation.ispartofKidney Internationalen_US
dc.subject.meshBlood Physiological Phenomenaen_US
dc.subject.meshCell Division - Physiologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCytoskeleton - Physiologyen_US
dc.subject.meshDialysis Solutions - Pharmacologyen_US
dc.subject.meshEpithelium - Drug Effects - Pathology - Physiopathologyen_US
dc.subject.meshExtracellular Matrix - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshPeritoneum - Drug Effects - Injuries - Pathology - Physiopathologyen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshWound Healing - Drug Effects - Physiologyen_US
dc.titleResponse of the human peritoneal mesothelial cell to injury: An in vitro model of peritoneal wound healingen_US
dc.typeConference_Paperen_US
dc.identifier.emailYung, S:ssyyung@hku.hken_US
dc.identifier.authorityYung, S=rp00455en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1046/j.1523-1755.1998.00177.xen_US
dc.identifier.pmid9853283-
dc.identifier.scopuseid_2-s2.0-0031786809en_US
dc.identifier.hkuros46254-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031786809&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume54en_US
dc.identifier.issue6en_US
dc.identifier.spage2160en_US
dc.identifier.epage2169en_US
dc.identifier.isiWOS:000077129000039-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridYung, S=22636568800en_US
dc.identifier.scopusauthoridDavies, M=7404207291en_US

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