dc.creatorGiannella, Maria Lucia Cardillo Correa
dc.creatorAndrade de Azevedo, Maria Regina
dc.creatorLeRoith, Derek
dc.creatorGiannella-Neto, Daniel
dc.date.accessioned2013-10-23T14:52:29Z
dc.date.accessioned2018-07-04T16:01:47Z
dc.date.available2013-10-23T14:52:29Z
dc.date.available2018-07-04T16:01:47Z
dc.date.created2013-10-23T14:52:29Z
dc.date.issued2012
dc.identifierDIABETOLOGY & METABOLIC SYNDROME, LONDON, v. 4, pp. 209-215, MAY 3, 2012
dc.identifier1758-5996
dc.identifierhttp://www.producao.usp.br/handle/BDPI/35758
dc.identifier10.1186/1758-5996-4-19
dc.identifierhttp://dx.doi.org/10.1186/1758-5996-4-19
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1630658
dc.description.abstractThe advanced glycation end products, namely AGEs, contribute to long-termed complications of diabetes mellitus, including macroangiopathy, where smooth muscle cells (SMC) proliferation stimulated by platelet-derived growth factor (PDGF) isoforms and insulin-like growth factor-I (IGF-I) plays an important role. The objective of the present study was to investigate the effect of an AGE-modified extracellular matrix protein on IGF-I induced SMC proliferation and on the IGF-I-IGF binding protein 4 (IGFBP-4) axis under basal conditions and after stimulation with PDGF-BB. IGF-I resulted in significantly higher thymidine incorporation in SMC seeded on AGE-modified fibronectin (AGE-FN) in comparison to cells seeded on fibronectin (FN). This augmented proliferation could not be accounted for by increased expression of IGF-IR, by decreased secretion of IGFBP-4, a binding protein that inhibits IGF-I mitogenic effects or by increased IGF-IR autophosphorylation. PDGF-BB did not modulate IGF-IR and IGFBP-4 mRNA expression in any of the substrata, however, this growth factor elicited opposite effects on the IGFBP-4 content in the conditioned media, increasing it in cells plated on FN and diminishing it in cells plated on AGE-FN. These findings suggest that one mechanism by which AGE-modified proteins is involved in the pathogenesis of diabetes-associated atherosclerosis might be by increasing SMC susceptibility to IGF-I mitogenic effects.
dc.languageeng
dc.publisherBIOMED CENTRAL LTD
dc.publisherLONDON
dc.relationDIABETOLOGY & METABOLIC SYNDROME
dc.rightsCopyright BIOMED CENTRAL LTD
dc.rightsopenAccess
dc.subjectDIABETES MELLITUS
dc.subjectADVANCED GLYCATION END PRODUCTS (AGE)
dc.subjectSMOOTH MUSCLE CELLS
dc.subjectPDGF
dc.subjectIGF-I
dc.subjectIGFBP-4
dc.titleFibronectin glycation increases IGF-I induced proliferation of human aortic smooth muscle cells
dc.typeArtículos de revistas


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