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
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/153966

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network_name_str SEDICI (UNLP)
spelling 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
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://sedici.unlp.edu.ar/handle/10915/153966
url http://sedici.unlp.edu.ar/handle/10915/153966
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/issn/1573-4919
info:eu-repo/semantics/altIdentifier/doi/10.1007/s11010-007-9557-8
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by/4.0/
Creative Commons Attribution 4.0 International (CC BY 4.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/4.0/
Creative Commons Attribution 4.0 International (CC BY 4.0)
dc.format.none.fl_str_mv application/pdf
87-94
dc.source.none.fl_str_mv reponame:SEDICI (UNLP)
instname:Universidad Nacional de La Plata
instacron:UNLP
reponame_str SEDICI (UNLP)
collection SEDICI (UNLP)
instname_str Universidad Nacional de La Plata
instacron_str UNLP
institution UNLP
repository.name.fl_str_mv SEDICI (UNLP) - Universidad Nacional de La Plata
repository.mail.fl_str_mv alira@sedici.unlp.edu.ar
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