Regulation of advanced glycation end product (AGE) receptors and apoptosis by AGEs in osteoblast-like cells
- Autores
- Mercer, Natalia; Ahmed, Hafiz; Etcheverry, Susana Beatriz; Vasta, Gerardo R.; Cortizo, Ana María
- Año de publicación
- 2007
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Advanced 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.
Laboratorio de Investigación en Osteopatías y Metabolismo Mineral - Materia
-
Biología
Advanced glycation end products
RAGE
Galectin-3
Osteoblasts
Apoptosis
AGE-receptors
Regulation - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by/4.0/
- Repositorio
.jpg)
- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/153966
Ver los metadatos del registro completo
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Regulation of advanced glycation end product (AGE) receptors and apoptosis by AGEs in osteoblast-like cellsMercer, NataliaAhmed, HafizEtcheverry, Susana BeatrizVasta, Gerardo R.Cortizo, Ana MaríaBiologíaAdvanced glycation end productsRAGEGalectin-3OsteoblastsApoptosisAGE-receptorsRegulationAdvanced 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.Laboratorio de Investigación en Osteopatías y Metabolismo Mineral2007-07-28info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf87-94http://sedici.unlp.edu.ar/handle/10915/153966enginfo:eu-repo/semantics/altIdentifier/issn/1573-4919info:eu-repo/semantics/altIdentifier/doi/10.1007/s11010-007-9557-8info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/Creative Commons Attribution 4.0 International (CC BY 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-11-12T11:04:13Zoai:sedici.unlp.edu.ar:10915/153966Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-11-12 11:04:13.99SEDICI (UNLP) - Universidad Nacional de La Platafalse |
| dc.title.none.fl_str_mv |
Regulation of advanced glycation end product (AGE) receptors and apoptosis by AGEs in osteoblast-like cells |
| title |
Regulation of advanced glycation end product (AGE) receptors and apoptosis by AGEs in osteoblast-like cells |
| spellingShingle |
Regulation of advanced glycation end product (AGE) receptors and apoptosis by AGEs in osteoblast-like cells Mercer, Natalia Biología Advanced glycation end products RAGE Galectin-3 Osteoblasts Apoptosis AGE-receptors Regulation |
| title_short |
Regulation of advanced glycation end product (AGE) receptors and apoptosis by AGEs in osteoblast-like cells |
| title_full |
Regulation of advanced glycation end product (AGE) receptors and apoptosis by AGEs in osteoblast-like cells |
| title_fullStr |
Regulation of advanced glycation end product (AGE) receptors and apoptosis by AGEs in osteoblast-like cells |
| title_full_unstemmed |
Regulation of advanced glycation end product (AGE) receptors and apoptosis by AGEs in osteoblast-like cells |
| title_sort |
Regulation of advanced glycation end product (AGE) receptors and apoptosis by AGEs in osteoblast-like cells |
| dc.creator.none.fl_str_mv |
Mercer, Natalia Ahmed, Hafiz Etcheverry, Susana Beatriz Vasta, Gerardo R. Cortizo, Ana María |
| author |
Mercer, Natalia |
| author_facet |
Mercer, Natalia Ahmed, Hafiz Etcheverry, Susana Beatriz Vasta, Gerardo R. Cortizo, Ana María |
| author_role |
author |
| author2 |
Ahmed, Hafiz Etcheverry, Susana Beatriz Vasta, Gerardo R. Cortizo, Ana María |
| author2_role |
author author author author |
| dc.subject.none.fl_str_mv |
Biología Advanced glycation end products RAGE Galectin-3 Osteoblasts Apoptosis AGE-receptors Regulation |
| topic |
Biología Advanced glycation end products RAGE Galectin-3 Osteoblasts Apoptosis AGE-receptors Regulation |
| dc.description.none.fl_txt_mv |
Advanced 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. Laboratorio de Investigación en Osteopatías y Metabolismo Mineral |
| description |
Advanced 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. |
| publishDate |
2007 |
| dc.date.none.fl_str_mv |
2007-07-28 |
| dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion Articulo http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
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article |
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publishedVersion |
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http://sedici.unlp.edu.ar/handle/10915/153966 |
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http://sedici.unlp.edu.ar/handle/10915/153966 |
| dc.language.none.fl_str_mv |
eng |
| language |
eng |
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info:eu-repo/semantics/altIdentifier/issn/1573-4919 info:eu-repo/semantics/altIdentifier/doi/10.1007/s11010-007-9557-8 |
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info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/4.0/ Creative Commons Attribution 4.0 International (CC BY 4.0) |
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openAccess |
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http://creativecommons.org/licenses/by/4.0/ Creative Commons Attribution 4.0 International (CC BY 4.0) |
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