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

Diabetology & Metabolic Syndrome

Daniel Giannella-Neto⁴  Derek LeRoith¹  Maria Regina Andrade de Azevedo³  Maria Lúcia Corrêa-Giannella² 

[1] Division of Endocrinology and Diabetes, Department of Medicine, The Mount Sinai School of Medicine, 1 Gustave Levy Place, Box 1055, New York, USA;Laboratory for Cellular and Molecular Endocrinology (LIM-25). Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, Av. Dr. Arnaldo, 455, Sala 4305, São Paulo, Brazil;Universidade Santo Amaro (UNISA), R. Enéas de Siqueira Neto, 340, São Paulo, Brazil;Laboratory for Clinical and Experimental Gastroenterology (LIM-07). Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, Av. Dr. Arnaldo, 455, Sala #4387, São Paulo, Brazil

关键词: IGFBP-4;    IGF-I;    PDGF;    Smooth muscle cells;    Advanced glycation end products (AGE);    Diabetes mellitus;   

Others  :  815074
DOI  :  10.1186/1758-5996-4-19

 received in 2011-06-21, accepted in 2012-04-09,  发布年份 2012

【 摘 要 】

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.

【 授权许可】

   
2012 Corrêa-Giannella et al.; licensee BioMed Central Ltd.

【 图 表 】

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