Regulation of advanced glycation end product (AGE) receptors and apoptosis by AGEs in osteoblast-like cells

dc.creatorMercer, Natalia
dc.creatorAhmed, Hafiz
dc.creatorEtcheverry, Susana Beatriz
dc.creatorVasta, Gerardo R.
dc.creatorCortizo, Ana María
dc.date2007-07-28
dc.date2023-06-05T18:43:15Z
dc.date.accessioned2023-07-15T10:45:29Z
dc.date.available2023-07-15T10:45:29Z
dc.identifierhttp://sedici.unlp.edu.ar/handle/10915/153966
dc.identifierissn:1573-4919
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/7493077
dc.descriptionAdvanced glycation end products (AGEs) have been proposed as the pathological mechanisms underlying diabetic chronic complications. They may also play a role in the pathogenesis of diabetic osteopenia, although their mechanisms of action remain unclear. We investigated the protein (immunofluorescence) and gene expression (realtime RT-PCR) of two receptors for AGEs, RAGE and galectin-3, as well as their regulation by AGEs, and the apoptotic effect on osteoblast-like cells (UMR106 and MC3T3E1) in culture. AGEs up-regulated the expression of RAGE and galectin-3 in both cells lines. These effects were accompanied by an increase in the corresponding mRNA in the non-tumoral MC3T3E1 but not in the osteosarcoma UMR106 cells. Finally, we demonstrated that a 24 h exposure to AGEs induced apoptosis in both cell lines. Thus, AGEs-receptors may play important roles in the bone alterations described in aging and diabetic patients.
dc.descriptionLaboratorio de Investigación en Osteopatías y Metabolismo Mineral
dc.formatapplication/pdf
dc.format87-94
dc.languageen
dc.rightshttp://creativecommons.org/licenses/by/4.0/
dc.rightsCreative Commons Attribution 4.0 International (CC BY 4.0)
dc.subjectBiología
dc.subjectAdvanced glycation end products
dc.subjectRAGE
dc.subjectGalectin-3
dc.subjectOsteoblasts
dc.subjectApoptosis
dc.subjectAGE-receptors
dc.subjectRegulation
dc.titleRegulation of advanced glycation end product (AGE) receptors and apoptosis by AGEs in osteoblast-like cells
dc.typeArticulo
dc.typeArticulo


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