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Fibronectin glycation increases IGF-I induced proliferation of human aortic smooth muscle cells.doc

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Fibronectin glycation increases IGF-I induced proliferation of human aortic smooth muscle cells

Corrêa-Giannellaetal.DiabetologyMetabolicSyndrome2012,4:19 /content/4/1/19 DIABETOLOGY METABOLIC SYNDROME RESEARCH OpenAccess FibronectinglycationincreasesIGF-Iinduced proliferationofhumanaorticsmoothmusclecells MariaLúciaCorrêa-Giannella1,MariaReginaAndradedeAzevedo2,DerekLeRoith3andDanielGiannella-Neto4* Abstract Theadvancedglycationendproducts,namelyAGEs,contributetolong-termedcomplicationsofdiabetesmellitus, includingmacroangiopathy,wheresmoothmusclecells(SMC)proliferationstimulatedbyplatelet-derivedgrowth factor(PDGF)isoformsandinsulin-likegrowthfactor-I(IGF-I)playsanimportantrole.Theobjectiveofthepresent studywastoinvestigatetheeffectofanAGE-modifiedextracellularmatrixproteinonIGF-IinducedSMC proliferationandontheIGF-I-IGFbindingprotein4(IGFBP-4)axisunderbasalconditionsandafterstimulationwith PDGF-BB.IGF-IresultedinsignificantlyhigherthymidineincorporationinSMCseededonAGE-modifiedfibronectin (AGE-FN)incomparisontocellsseededonfibronectin(FN).Thisaugmentedproliferationcouldnotbeaccounted forbyincreasedexpressionofIGF-IR,bydecreasedsecretionofIGFBP-4,abindingproteinthatinhibitsIGF-I mitogeniceffectsorbyincreasedIGF-IRautophosphorylation.PDGF-BBdidnotmodulateIGF-IRandIGFBP-4mRNA expressioninanyofthesubstrata,however,thisgrowthfactorelicitedoppositeeffectsontheIGFBP-4contentin theconditionedmedia,increasingitincellsplatedonFNanddiminishingitincellsplatedonAGE-FN.These findingssuggestthatonemechanismbywhichAGE-modifiedproteinsisinvolvedinthepathogenesisofdiabetes- associatedatherosclerosismightbebyincreasingSMCsusceptibilitytoIGF-Imitogeniceffects. Keywords:Diabetesmellitus,Advancedglycationendproducts(AGE),Smoothmusclecells,PDGF,IGF-I,IGFBP-4 Background synthesisandsecretionofcytokinesandgrowthfactorsafter BothtypeIandtypeIIdiabetesarepowerfulandindepend- bindingtoAGEreceptors(RAGE)indifferentcelltypes[7]. entriskfactorsforcoronaryarterydisease,stroke,andper- MonocytesexposedtoAGE-modifiedmatrixreleasetumor ipheral arterial disease [1,2]. Prolong