File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Differential expression of receptors for advanced glycation end-products in peritoneal mesothelial cells exposed to glucose degradation products

TitleDifferential expression of receptors for advanced glycation end-products in peritoneal mesothelial cells exposed to glucose degradation products
Authors
KeywordsAdvanced glycation end-products
Glucose degradation products
Peritoneal dialysis peritoneal mesothelial cells
Receptor
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. 138 n. 3, p. 466-475 How to Cite?
AbstractAutoclaving peritoneal dialysate fluid (PDF) degrades glucose into glucose degradation products (GDPs) that impair peritoneal mesothelial cell functions. While glycation processes leading to formation of advanced glycation end-products (AGE) were viewed commonly as being mediated by glucose present in the PDF, recent evidence indicates that certain GDPs are even more powerful inducers of AGE formation than glucose per se. In the present study, we examined the expression and modulation of AGE receptors on human peritoneal mesothelial cells (HPMC) cultured with GDPs, conventional PDF or PDF with low GDP content. HPMC cultured with GDPs differentially modulated AGE receptors (including RAGE, AGE-R1, AGE-R2 and AGE-R3) expression in a dose-dependent manner. At subtoxic concentrations, GDPs increased RAGE mRNA expression in HPMC. 2-furaldehyde (FurA), methylglyoxal (M-Glx) and 3,4-dideoxy-glucosone-3-Ene (3,4-DGE) increased the expression of AGE-R1 and RAGE, the receptors that are associated with toxic effects. These three GDPs up-regulated the AGE synthesis by cultured HPMC. In parallel, these GDPs also increased the expression of vascular endothelial growth factor (VEGF) in HPMC. PDF with lower GDP content exerted less cytotoxic effect than traditional heat-sterilized PDF. Both PDF preparations up-regulated the protein expression of RAGE and VEGF. However, the up-regulation of VEGF in HPMC following 24-h culture with conventional PDF was higher than values from HPMC cultured with PDF containing low GDP. We have demonstrated, for the first time, that in addition to RAGE, other AGE receptors including AGE-R1, AGE-R2 and AGE-R3 are expressed on HPMC. Different GDPs exert differential regulation on the expression of these receptors on HPMC. The interactions between GDPs and AGE receptors may bear biological relevance to the intraperitoneal homeostasis and membrane integrity.
Persistent Identifierhttp://hdl.handle.net/10722/49141
ISSN
2015 Impact Factor: 3.148
2015 SCImago Journal Rankings: 1.369
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorLi, FFKen_HK
dc.contributor.authorTang, SCWen_HK
dc.contributor.authorLam, MFen_HK
dc.contributor.authorTse, KCen_HK
dc.contributor.authorYip, TPen_HK
dc.contributor.authorChan, TMen_HK
dc.contributor.authorWieslander, Aen_HK
dc.contributor.authorVlassara, Hen_HK
dc.date.accessioned2008-06-12T06:35:18Z-
dc.date.available2008-06-12T06:35:18Z-
dc.date.issued2004en_HK
dc.identifier.citationClinical And Experimental Immunology, 2004, v. 138 n. 3, p. 466-475en_HK
dc.identifier.issn0009-9104en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49141-
dc.description.abstractAutoclaving peritoneal dialysate fluid (PDF) degrades glucose into glucose degradation products (GDPs) that impair peritoneal mesothelial cell functions. While glycation processes leading to formation of advanced glycation end-products (AGE) were viewed commonly as being mediated by glucose present in the PDF, recent evidence indicates that certain GDPs are even more powerful inducers of AGE formation than glucose per se. In the present study, we examined the expression and modulation of AGE receptors on human peritoneal mesothelial cells (HPMC) cultured with GDPs, conventional PDF or PDF with low GDP content. HPMC cultured with GDPs differentially modulated AGE receptors (including RAGE, AGE-R1, AGE-R2 and AGE-R3) expression in a dose-dependent manner. At subtoxic concentrations, GDPs increased RAGE mRNA expression in HPMC. 2-furaldehyde (FurA), methylglyoxal (M-Glx) and 3,4-dideoxy-glucosone-3-Ene (3,4-DGE) increased the expression of AGE-R1 and RAGE, the receptors that are associated with toxic effects. These three GDPs up-regulated the AGE synthesis by cultured HPMC. In parallel, these GDPs also increased the expression of vascular endothelial growth factor (VEGF) in HPMC. PDF with lower GDP content exerted less cytotoxic effect than traditional heat-sterilized PDF. Both PDF preparations up-regulated the protein expression of RAGE and VEGF. However, the up-regulation of VEGF in HPMC following 24-h culture with conventional PDF was higher than values from HPMC cultured with PDF containing low GDP. We have demonstrated, for the first time, that in addition to RAGE, other AGE receptors including AGE-R1, AGE-R2 and AGE-R3 are expressed on HPMC. Different GDPs exert differential regulation on the expression of these receptors on HPMC. The interactions between GDPs and AGE receptors may bear biological relevance to the intraperitoneal homeostasis and membrane integrity.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.rightsClinical and Experimental Immunology. Copyright © Blackwell Publishing Ltd.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsThe definitive version is available at www.blackwell-synergy.comen_HK
dc.subjectAdvanced glycation end-productsen_HK
dc.subjectGlucose degradation productsen_HK
dc.subjectPeritoneal dialysis peritoneal mesothelial cellsen_HK
dc.subjectReceptoren_HK
dc.titleDifferential expression of receptors for advanced glycation end-products in peritoneal mesothelial cells exposed to glucose degradation productsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0009-9104&volume=138&issue=3&spage=466&epage=475&date=2004&atitle=Differential+expression+of+receptors+for+advanced+glycation+end-products+in+peritoneal+mesothelial+cells+exposed+to+glucose+degradation+productsen_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailTang, SCW: scwtang@hku.hken_HK
dc.identifier.emailChan, TM: dtmchan@hku.hken_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityTang, SCW=rp00480en_HK
dc.identifier.authorityChan, TM=rp00394en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1111/j.1365-2249.2004.02629.xen_HK
dc.identifier.pmid15544624-
dc.identifier.pmcidPMC1809241en_HK
dc.identifier.scopuseid_2-s2.0-9644266522en_HK
dc.identifier.hkuros99277-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-9644266522&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume138en_HK
dc.identifier.issue3en_HK
dc.identifier.spage466en_HK
dc.identifier.epage475en_HK
dc.identifier.isiWOS:000225079700013-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridChan, LYY=8108378300en_HK
dc.identifier.scopusauthoridLi, FFK=55210612400en_HK
dc.identifier.scopusauthoridTang, SCW=7403437082en_HK
dc.identifier.scopusauthoridLam, MF=35300050600en_HK
dc.identifier.scopusauthoridTse, KC=7102609864en_HK
dc.identifier.scopusauthoridYip, TP=7004283977en_HK
dc.identifier.scopusauthoridChan, TM=7402687700en_HK
dc.identifier.scopusauthoridWieslander, A=7005892114en_HK
dc.identifier.scopusauthoridVlassara, H=7005741880en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats