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Article: Pathophysiology of the peritoneal membrane during peritoneal dialysis: the role of hyaluronan

TitlePathophysiology of the peritoneal membrane during peritoneal dialysis: the role of hyaluronan
Authors
Issue Date2011
PublisherHindawi Publishing Corporation. The Journal's web site is located at http://www.hindawi.com/journals/jbb/index.html
Citation
Journal of Biomedicine and Biotechnology, 2011, v. 2011, article no. 180594 How to Cite?
AbstractDuring peritoneal dialysis (PD), constant exposure of mesothelial cells to bioincompatible PD solutions results in the denudation of the mesothelial monolayer and impairment of mesothelial cell function. Hyaluronan, a major component of extracellular matrices, is synthesized by mesothelial cells and contributes to remesothelialization, maintenance of cell phenotype, and tissue remodeling and provides structural support to the peritoneal membrane. Chronic peritoneal inflammation is observed in long-term PD patients and is associated with increased hyaluronan synthesis. During inflammation, depolymerization of hyaluronan may occur with the generation of hyaluronan fragments. In contrast to native hyaluronan which offers a protective role to the peritoneum, hyaluronan fragments exacerbate inflammatory and fibrotic processes and therefore assist in the destruction of the tissue. This paper will discuss the contribution of mesothelial cells to peritoneal membrane alterations that are induced by PD and the putative role of hyaluronan in these processes.
Persistent Identifierhttp://hdl.handle.net/10722/159690
ISSN
2014 Impact Factor: 3.169
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYung, Sen_US
dc.contributor.authorChan, TMen_US
dc.date.accessioned2012-08-16T05:54:04Z-
dc.date.available2012-08-16T05:54:04Z-
dc.date.issued2011en_US
dc.identifier.citationJournal of Biomedicine and Biotechnology, 2011, v. 2011, article no. 180594en_US
dc.identifier.issn1110-7243-
dc.identifier.urihttp://hdl.handle.net/10722/159690-
dc.description.abstractDuring peritoneal dialysis (PD), constant exposure of mesothelial cells to bioincompatible PD solutions results in the denudation of the mesothelial monolayer and impairment of mesothelial cell function. Hyaluronan, a major component of extracellular matrices, is synthesized by mesothelial cells and contributes to remesothelialization, maintenance of cell phenotype, and tissue remodeling and provides structural support to the peritoneal membrane. Chronic peritoneal inflammation is observed in long-term PD patients and is associated with increased hyaluronan synthesis. During inflammation, depolymerization of hyaluronan may occur with the generation of hyaluronan fragments. In contrast to native hyaluronan which offers a protective role to the peritoneum, hyaluronan fragments exacerbate inflammatory and fibrotic processes and therefore assist in the destruction of the tissue. This paper will discuss the contribution of mesothelial cells to peritoneal membrane alterations that are induced by PD and the putative role of hyaluronan in these processes.-
dc.languageengen_US
dc.publisherHindawi Publishing Corporation. The Journal's web site is located at http://www.hindawi.com/journals/jbb/index.html-
dc.relation.ispartofJournal of Biomedicine and Biotechnologyen_US
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subject.meshDialysis Solutions - adverse effects-
dc.subject.meshEpithelial Cells - metabolism - secretion-
dc.subject.meshHyaluronic Acid - metabolism - secretion-
dc.subject.meshPeritoneal Dialysis - adverse effects-
dc.subject.meshPeritoneum - physiopathology-
dc.titlePathophysiology of the peritoneal membrane during peritoneal dialysis: the role of hyaluronanen_US
dc.typeArticleen_US
dc.identifier.emailYung, S: ssyyung@hku.hken_US
dc.identifier.emailChan, TM: dtmchan@hku.hken_US
dc.identifier.authorityYung, SSY=rp00455en_US
dc.identifier.authorityChan, DTM=rp00394en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1155/2011/180594-
dc.identifier.pmid22203782-
dc.identifier.pmcidPMC3238805-
dc.identifier.scopuseid_2-s2.0-84855554053-
dc.identifier.hkuros204924en_US
dc.identifier.volume2011, article no. 180594-
dc.identifier.isiWOS:000298679800001-
dc.publisher.placeUnited States-
dc.identifier.issnl1110-7243-

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