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Article: Induction of hyaluronan metabolism after mechanical injury of human peritoneal mesothelial cells in vitro

TitleInduction of hyaluronan metabolism after mechanical injury of human peritoneal mesothelial cells in vitro
Authors
Issue Date2000
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.html
Citation
Kidney International, 2000, v. 58 n. 5, p. 1953-1962 How to Cite?
AbstractBackground. Hyaluronan (HA) is an important extracellular matrix component that is involved in cell movement and tissue repair. In vertebrates, HA synthase genes (HAS 1, HAS 2, and HAS 3) that control the synthesis of HA have been identified. In this article, we investigated HA synthesis in the response of human peritoneal mesothelial cells (HPMCs) to injury. Methods. The expression of HAS 1, HAS 2, and HAS 3 mRNA and the synthesis of [ 3H]-labeled HA were examined in an in vitro model of peritoneal mesothelial cell damage. The staining for uridine diphosphoglucose dehydrogenase, a key enzyme in the synthesis of HA, and biotinylated HA-binding protein was used to determine the cellular location of HA synthesis and its site of deposition. Results. Growth-arrested human HPMCs expressed low levels of mRNA for HAS 2 and HAS 3 but not HAS 1. Following injury to the monolayer, HAS 2 was up-regulated by 6 hours, reaching maximal expression between 12 and 24 hours. In contrast, the expression of HAS 3 was down-regulated. During the same time period, synthesis of HA was increased in the injured monolayer. This synthetic activity appeared to be restricted to cells at the edge of the wound and to cells entering the wound. In a separate series of experiments, the addition of HA to the injured monolayer at a concentration range found in peritoneal fluid (50 to 3300 ng/mL) increased the migration of cells into the wound in a dose-dependent manner. Conclusions. These studies provide evidence that HA is an important component of peritoneal mesothelial cell migration. The results also suggest that in this process, there is differential regulation of HAS gene expression and that the synthesis of HA is limited to cells located at the leading edge of the wound.
Persistent Identifierhttp://hdl.handle.net/10722/162373
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.authorThomas, GJen_US
dc.contributor.authorDavies, Men_US
dc.date.accessioned2012-09-05T05:19:21Z-
dc.date.available2012-09-05T05:19:21Z-
dc.date.issued2000en_US
dc.identifier.citationKidney International, 2000, v. 58 n. 5, p. 1953-1962en_US
dc.identifier.issn0085-2538en_US
dc.identifier.urihttp://hdl.handle.net/10722/162373-
dc.description.abstractBackground. Hyaluronan (HA) is an important extracellular matrix component that is involved in cell movement and tissue repair. In vertebrates, HA synthase genes (HAS 1, HAS 2, and HAS 3) that control the synthesis of HA have been identified. In this article, we investigated HA synthesis in the response of human peritoneal mesothelial cells (HPMCs) to injury. Methods. The expression of HAS 1, HAS 2, and HAS 3 mRNA and the synthesis of [ 3H]-labeled HA were examined in an in vitro model of peritoneal mesothelial cell damage. The staining for uridine diphosphoglucose dehydrogenase, a key enzyme in the synthesis of HA, and biotinylated HA-binding protein was used to determine the cellular location of HA synthesis and its site of deposition. Results. Growth-arrested human HPMCs expressed low levels of mRNA for HAS 2 and HAS 3 but not HAS 1. Following injury to the monolayer, HAS 2 was up-regulated by 6 hours, reaching maximal expression between 12 and 24 hours. In contrast, the expression of HAS 3 was down-regulated. During the same time period, synthesis of HA was increased in the injured monolayer. This synthetic activity appeared to be restricted to cells at the edge of the wound and to cells entering the wound. In a separate series of experiments, the addition of HA to the injured monolayer at a concentration range found in peritoneal fluid (50 to 3300 ng/mL) increased the migration of cells into the wound in a dose-dependent manner. Conclusions. These studies provide evidence that HA is an important component of peritoneal mesothelial cell migration. The results also suggest that in this process, there is differential regulation of HAS gene expression and that the synthesis of HA is limited to cells located at the leading edge of the wound.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.meshCell Movement - Drug Effectsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshEpithelium - Injuries - Metabolism - Pathology - Physiopathologyen_US
dc.subject.meshGlucuronosyltransferase - Metabolismen_US
dc.subject.meshGlycosyltransferasesen_US
dc.subject.meshHumansen_US
dc.subject.meshHyaluronic Acid - Biosynthesis - Metabolismen_US
dc.subject.meshMembrane Proteinsen_US
dc.subject.meshPeritoneum - Injuries - Metabolism - Pathology - Physiopathologyen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshTissue Distributionen_US
dc.subject.meshTransferasesen_US
dc.subject.meshWound Healing - Drug Effectsen_US
dc.subject.meshWounds And Injuries - Metabolism - Pathology - Physiopathologyen_US
dc.subject.meshXenopus Proteinsen_US
dc.titleInduction of hyaluronan metabolism after mechanical injury of human peritoneal mesothelial cells in vitroen_US
dc.typeArticleen_US
dc.identifier.emailYung, S:ssyyung@hku.hken_US
dc.identifier.authorityYung, S=rp00455en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1046/j.1523-1755.2000.00367.xen_US
dc.identifier.pmid11044215-
dc.identifier.scopuseid_2-s2.0-0033753655en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033753655&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume58en_US
dc.identifier.issue5en_US
dc.identifier.spage1953en_US
dc.identifier.epage1962en_US
dc.identifier.isiWOS:000090154500013-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridYung, S=22636568800en_US
dc.identifier.scopusauthoridThomas, GJ=35464458200en_US
dc.identifier.scopusauthoridDavies, M=7404207291en_US

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