File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Regulation of complement C3 and C4 synthesis in human peritoneal mesothelial cells by peritoneal dialysis fluid

TitleRegulation of complement C3 and C4 synthesis in human peritoneal mesothelial cells by peritoneal dialysis fluid
Authors
KeywordsComplement
Human peritoneal mesothelial cells
Hypertonic glucose
Mannitol
Peritoneal defence
Peritoneal dialysis
Issue Date2004
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEI
Citation
Clinical and Experimental Immunology, 2004, v. 136 n. 1, p. 85-94 How to Cite?
AbstractAlthough complement is activated in the peritoneal cavity during chronic peritoneal dialysis (PD), little is known about its role in peritoneal defence and injury related to long-term PD. We examined the impact of glucose and commercial peritoneal dialysis solutions on complement expression in HPMCs obtained by primary culture from omental tissues of consented patients undergoing elective abdominal surgery. Constitutive expression of C3 and C4 mRNA in HPMCs was up-regulated upon exposure to 75 mM glucose in a time-dependent manner. C3 and C4 protein was secreted in both apical and basolateral directions. Glucose doses beyond 100 mM markedly down-regulated C3 and C4 expression, and stimulated LDH release dose-dependently. Such cytotoxic effects were attenuated using equivalent doses of mannitol instead of glucose. Treatment with conventional lactate-buffered dialysis solution gave rise to down-regulation of C3 and C4 expression, and heightened LDH release in HPMCs. These effects correlated with the glucose strength of the solution, persisted despite replacement with a bicarbonate-buffered solution, aggravated by glycated albumin, and were partially abrogated by supplementation with 10% fetal bovine serum in the culture system. Our findings suggest that the artificial conditions imposed by PD lead to alterations in local complement synthesis that have implications for the role of the peritoneal mesothelium in both inflammation and defence.
Persistent Identifierhttp://hdl.handle.net/10722/49128
ISSN
2021 Impact Factor: 5.732
2020 SCImago Journal Rankings: 1.329
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTang, Sen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorTsang, AWLen_HK
dc.contributor.authorChen, CXRen_HK
dc.contributor.authorZhou, Wen_HK
dc.contributor.authorLai, KNen_HK
dc.contributor.authorSacks, SHen_HK
dc.date.accessioned2008-06-12T06:35:01Z-
dc.date.available2008-06-12T06:35:01Z-
dc.date.issued2004en_HK
dc.identifier.citationClinical and Experimental Immunology, 2004, v. 136 n. 1, p. 85-94en_HK
dc.identifier.issn0009-9104en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49128-
dc.description.abstractAlthough complement is activated in the peritoneal cavity during chronic peritoneal dialysis (PD), little is known about its role in peritoneal defence and injury related to long-term PD. We examined the impact of glucose and commercial peritoneal dialysis solutions on complement expression in HPMCs obtained by primary culture from omental tissues of consented patients undergoing elective abdominal surgery. Constitutive expression of C3 and C4 mRNA in HPMCs was up-regulated upon exposure to 75 mM glucose in a time-dependent manner. C3 and C4 protein was secreted in both apical and basolateral directions. Glucose doses beyond 100 mM markedly down-regulated C3 and C4 expression, and stimulated LDH release dose-dependently. Such cytotoxic effects were attenuated using equivalent doses of mannitol instead of glucose. Treatment with conventional lactate-buffered dialysis solution gave rise to down-regulation of C3 and C4 expression, and heightened LDH release in HPMCs. These effects correlated with the glucose strength of the solution, persisted despite replacement with a bicarbonate-buffered solution, aggravated by glycated albumin, and were partially abrogated by supplementation with 10% fetal bovine serum in the culture system. Our findings suggest that the artificial conditions imposed by PD lead to alterations in local complement synthesis that have implications for the role of the peritoneal mesothelium in both inflammation and defence.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEIen_HK
dc.relation.ispartofClinical and Experimental Immunologyen_HK
dc.subjectComplementen_HK
dc.subjectHuman peritoneal mesothelial cellsen_HK
dc.subjectHypertonic glucoseen_HK
dc.subjectMannitolen_HK
dc.subjectPeritoneal defenceen_HK
dc.subjectPeritoneal dialysisen_HK
dc.titleRegulation of complement C3 and C4 synthesis in human peritoneal mesothelial cells by peritoneal dialysis fluiden_HK
dc.typeArticleen_HK
dc.identifier.emailTang, S: scwtang@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityTang, S=rp00480en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_OA_fulltexten_HK
dc.identifier.doi10.1111/j.1365-2249.2004.02407.xen_HK
dc.identifier.pmid15030518en_HK
dc.identifier.pmcidPMC1808994en_HK
dc.identifier.scopuseid_2-s2.0-1842559678en_HK
dc.identifier.hkuros86754-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1842559678&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume136en_HK
dc.identifier.issue1en_HK
dc.identifier.spage85en_HK
dc.identifier.epage94en_HK
dc.identifier.isiWOS:000220306300013-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridTang, S=7403437082en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridChan, LYY=8108378300en_HK
dc.identifier.scopusauthoridTsang, AWL=7006979244en_HK
dc.identifier.scopusauthoridChen, CXR=7501945199en_HK
dc.identifier.scopusauthoridZhou, W=7404515807en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridSacks, SH=7103294121en_HK
dc.identifier.issnl0009-9104-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats