dc.creator | Giannella, Maria Lucia Cardillo Correa | |
dc.creator | Andrade de Azevedo, Maria Regina | |
dc.creator | LeRoith, Derek | |
dc.creator | Giannella-Neto, Daniel | |
dc.date.accessioned | 2013-10-23T14:52:29Z | |
dc.date.accessioned | 2018-07-04T16:01:47Z | |
dc.date.available | 2013-10-23T14:52:29Z | |
dc.date.available | 2018-07-04T16:01:47Z | |
dc.date.created | 2013-10-23T14:52:29Z | |
dc.date.issued | 2012 | |
dc.identifier | DIABETOLOGY & METABOLIC SYNDROME, LONDON, v. 4, pp. 209-215, MAY 3, 2012 | |
dc.identifier | 1758-5996 | |
dc.identifier | http://www.producao.usp.br/handle/BDPI/35758 | |
dc.identifier | 10.1186/1758-5996-4-19 | |
dc.identifier | http://dx.doi.org/10.1186/1758-5996-4-19 | |
dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/1630658 | |
dc.description.abstract | The 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.language | eng | |
dc.publisher | BIOMED CENTRAL LTD | |
dc.publisher | LONDON | |
dc.relation | DIABETOLOGY & METABOLIC SYNDROME | |
dc.rights | Copyright BIOMED CENTRAL LTD | |
dc.rights | openAccess | |
dc.subject | DIABETES MELLITUS | |
dc.subject | ADVANCED GLYCATION END PRODUCTS (AGE) | |
dc.subject | SMOOTH MUSCLE CELLS | |
dc.subject | PDGF | |
dc.subject | IGF-I | |
dc.subject | IGFBP-4 | |
dc.title | Fibronectin glycation increases IGF-I induced proliferation of human aortic smooth muscle cells | |
dc.type | Artículos de revistas | |