Involvement of AP-1 in p38MAPK signaling pathway in osteoblast apoptosis induced by high glucose.
Genet Mol Res
; 14(2): 3149-59, 2015 Apr 10.
Article
en En
| MEDLINE
| ID: mdl-25966080
We investigated the effect of p38MAPK/AP-1 (activator protein-1) signaling on the apoptosis of osteoblasts induced by high glucose. A lentivirus vector of small hairpin RNA (shRNA) targeting p38MAPK was constructed in vitro. Osteoblasts MC3T3-E1 cultured in vitro were treated with vehicle, high glucose, p38MAPK-shRNA transfection, p38MAPK inhibitor, and unrelated shRNA transfection. Apoptosis, protein levels of p38MAPK, and activities of AP-1 in MC3T3-E1 osteoblasts were measured using TUNEL and flow cytometry, Western blot analysis, and an electrophoretic mobility shift assay. Compared with the vehicle group, high glucose induced apoptosis of MC3T3-E1 osteoblasts and activated p38MAPK and AP-1. p38MAPK-shRNA transfection blocked the effect of high glucose stimulation, and the p38MAPK inhibitor showed similar effects as those observed in p38MAPK transfection. Unrelated shRNA had no effect on these changes in MC3T3-E1 osteoblasts induced by high glucose. Therefore, our results suggest that p38MAPK-shRNA reduce apoptosis of MC3T3-E1 osteoblasts induced by high glucose by inhibiting the p38MAPK-AP-1 signaling pathway.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Osteoblastos
/
Transducción de Señal
/
Apoptosis
/
Factor de Transcripción AP-1
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Proteínas Quinasas p38 Activadas por Mitógenos
/
Glucosa
Límite:
Animals
Idioma:
En
Revista:
Genet Mol Res
Asunto de la revista:
BIOLOGIA MOLECULAR
/
GENETICA
Año:
2015
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Brasil