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Article: Interaction between the polyol pathway and non-enzymatic glycation on aortic smooth muscle cell migration and monocyte adhesion

TitleInteraction between the polyol pathway and non-enzymatic glycation on aortic smooth muscle cell migration and monocyte adhesion
Authors
KeywordsAdvanced glycation end-products (AGEs)
Aldose reductase gene
Diabetic atherosclerosis
Transgenic mouse
Issue Date2004
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 2004, v. 76 n. 4, p. 445-459 How to Cite?
AbstractWe investigated for the interaction between the polyol pathway and enhanced non-enzymatic glycation, both implicated in the pathogenesis of diabetic atherosclerosis, in the activation of aortic smooth muscle cell (SMC) function. Mouse aortas and primary cultures of SMCs from wildtype (WT) mice and transgenic (TG) mice expressing human aldose reductase (AR) were studied regarding changes in AR activity, and SMC gene activation, migration and monocyte adhesion, in response to advanced glycation end-product modified BSA (AGE-BSA). Results showed that AGE-BSA increased AR activity in both WT and TG aortas, with greater increments (p < 0.05) in TG aortas which, basally, had elevated AR activity (2.8 fold of WT). These increments were attenuated by zopolrestat, an AR inhibitor. Similar AGE-induced increments in AR activity were observed in primary cultures of aortic SMCs from WT and TG mice (60% and 100%, respectively, P < 0.01). Such increments were accompanied by increases in intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) mRNA levels (both P < 0.05), activation of membrane-associated PKC-β1 (P < 0.05) as well as increased SMC migration and Tamm-Horsfall protein (THP)-1 monocyte adhesion to SMCs (both p < 0.01), with all changes being significantly greater in TG SMCs (P < 0.05) and suppressible by either zopolrestat or transfection with an AR antisense oligonucleotide. Our findings suggest that the effects of AGEs on SMC activation, migration and monocyte adhesion are mediated partly through the polyol pathway and, possibly, PKC activation. The greater AGE-induced changes in the TG SMCs have provided further support for the dependency of such changes on polyol pathway hyperactivity. © 2004 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/78626
ISSN
2015 Impact Factor: 2.685
2015 SCImago Journal Rankings: 1.056
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDan, Qen_HK
dc.contributor.authorWong, Ren_HK
dc.contributor.authorChung, SKen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorLam, KSLen_HK
dc.date.accessioned2010-09-06T07:44:58Z-
dc.date.available2010-09-06T07:44:58Z-
dc.date.issued2004en_HK
dc.identifier.citationLife Sciences, 2004, v. 76 n. 4, p. 445-459en_HK
dc.identifier.issn0024-3205en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78626-
dc.description.abstractWe investigated for the interaction between the polyol pathway and enhanced non-enzymatic glycation, both implicated in the pathogenesis of diabetic atherosclerosis, in the activation of aortic smooth muscle cell (SMC) function. Mouse aortas and primary cultures of SMCs from wildtype (WT) mice and transgenic (TG) mice expressing human aldose reductase (AR) were studied regarding changes in AR activity, and SMC gene activation, migration and monocyte adhesion, in response to advanced glycation end-product modified BSA (AGE-BSA). Results showed that AGE-BSA increased AR activity in both WT and TG aortas, with greater increments (p < 0.05) in TG aortas which, basally, had elevated AR activity (2.8 fold of WT). These increments were attenuated by zopolrestat, an AR inhibitor. Similar AGE-induced increments in AR activity were observed in primary cultures of aortic SMCs from WT and TG mice (60% and 100%, respectively, P < 0.01). Such increments were accompanied by increases in intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) mRNA levels (both P < 0.05), activation of membrane-associated PKC-β1 (P < 0.05) as well as increased SMC migration and Tamm-Horsfall protein (THP)-1 monocyte adhesion to SMCs (both p < 0.01), with all changes being significantly greater in TG SMCs (P < 0.05) and suppressible by either zopolrestat or transfection with an AR antisense oligonucleotide. Our findings suggest that the effects of AGEs on SMC activation, migration and monocyte adhesion are mediated partly through the polyol pathway and, possibly, PKC activation. The greater AGE-induced changes in the TG SMCs have provided further support for the dependency of such changes on polyol pathway hyperactivity. © 2004 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescieen_HK
dc.relation.ispartofLife Sciencesen_HK
dc.subjectAdvanced glycation end-products (AGEs)en_HK
dc.subjectAldose reductase geneen_HK
dc.subjectDiabetic atherosclerosisen_HK
dc.subjectTransgenic mouseen_HK
dc.subject.meshAldehyde Reductase - antagonists & inhibitors - genetics - metabolismen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAntigens, CD - genetics - metabolismen_HK
dc.subject.meshAorta, Thoracic - drug effects - metabolismen_HK
dc.subject.meshBenzothiazolesen_HK
dc.subject.meshBlotting, Northernen_HK
dc.subject.meshCell Adhesion - drug effectsen_HK
dc.subject.meshCell Adhesion Molecules - genetics - metabolismen_HK
dc.subject.meshCell Movement - drug effectsen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshChemokine CCL2 - genetics - metabolismen_HK
dc.subject.meshEnzyme Inhibitors - pharmacologyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGlycosylation End Products, Advanced - pharmacologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Transgenicen_HK
dc.subject.meshMonocytes - cytology - drug effectsen_HK
dc.subject.meshMuscle, Smooth, Vascular - drug effects - metabolismen_HK
dc.subject.meshNerve Tissue Proteins - genetics - metabolismen_HK
dc.subject.meshOligoribonucleotides, Antisense - pharmacologyen_HK
dc.subject.meshPhthalazines - pharmacologyen_HK
dc.subject.meshPolymers - metabolismen_HK
dc.subject.meshRNA, Messenger - metabolismen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshSerum Albumin, Bovine - pharmacologyen_HK
dc.subject.meshThiazoles - pharmacologyen_HK
dc.titleInteraction between the polyol pathway and non-enzymatic glycation on aortic smooth muscle cell migration and monocyte adhesionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0885-1573&volume=76&issue=4&spage=445&epage=59&date=2004&atitle=Interaction+between+the+polyol+pathway+and+non-enzymatic+glycation+on+aortic+smooth+muscle+cell+migration+and+monocyte+adhesionen_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.lfs.2004.09.010en_HK
dc.identifier.pmid15530506-
dc.identifier.scopuseid_2-s2.0-7644241006en_HK
dc.identifier.hkuros98204en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-7644241006&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume76en_HK
dc.identifier.issue4en_HK
dc.identifier.spage445en_HK
dc.identifier.epage459en_HK
dc.identifier.isiWOS:000225137400009-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridDan, Q=8570225000en_HK
dc.identifier.scopusauthoridWong, R=37062742700en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK

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