dc.creatorSchurman, León
dc.creatorMcCarthy, Antonio Desmond
dc.creatorSedlinsky, Claudia
dc.creatorGangoiti, Maria Virginia
dc.creatorArnol, Verónica
dc.creatorBruzzone, Liliana
dc.creatorCortizo, Ana María
dc.date2007
dc.date.accessioned2023-08-31T00:52:13Z
dc.date.available2023-08-31T00:52:13Z
dc.identifierhttps://digital.cic.gba.gob.ar/handle/11746/11951
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8543851
dc.descriptionAdvanced glycation endproducts (AGEs) are implicated in the complications of diabetes and ageing, affecting several tissues, including bone. Metformin, an insulin-sensitizer drug, reduces the risk of life-threatening macrovascular complications. We have evaluated the hypothesis that metformin can abrogate AGE-induced deleterious effects in osteoblastic cells in culture. In two osteoblast-like cell lines (UMR106 and MC3T3E1), AGE-modifi ed albumin induced cell death, caspase- 3 activity, altered intracellular oxidative stress and inhibited alkaline phosphatase activity. Metformin-treatment of osteoblastic cells prevented these AGE-induced alterations. We also assessed the expression of AGE receptors as a possible mechanism by which metformin could modulate the action of AGEs. AGEs-treatment of osteoblast-like cells enhanced RAGE protein expression, and this up-regulation was prevented in the presence of metformin. Although the precise mechanisms involved in metformin signaling are still elusive, our data implicate the AGE-RAGE interaction in the modulation of growth and differentiation of osteoblastic cells.
dc.formatapplication/pdf
dc.format333-340
dc.languageInglés
dc.relationDOI: 0.1055/s-2007-992786
dc.relationISSN: 0947-7349
dc.rightshttp://creativecommons.org/licenses/by-nc-sa/4.0/
dc.subjectBioquímica y Biología Molecular
dc.subjectMetformin
dc.subjectAdvanced glycation end product
dc.subjectOsteoblasts
dc.subjectOxidative stress
dc.subjectRAGO
dc.titleMetformin Reverts Deleterious Effects of Advanced Glycation End-Products (AGEs) on Osteoblastic Cells


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