Peroxiredoxin I deficiency increases pancreatic ßcell apoptosis after streptozotocin stimulation via the AKT/GSK3ß signaling pathway.
Mol Med Rep
; 22(3): 1831-1838, 2020 09.
Article
en En
| MEDLINE
| ID: mdl-32705184
ABSTRACT
Apoptosis of pancreatic ßcells is involved in the pathogenesis of type I and II diabetes. Peroxiredoxin I (Prx I) serves an important role in regulating cellular apoptosis; however, the role of Prx I in pancreatic ßcell apoptosis is not completely understood. In the present study, the role of peroxiredoxin 1 (Prx I) during streptozotocin (STZ)induced apoptosis of pancreatic ßcells was investigated. The expression level of Prx I was decreased by STZ treatment in a timedependent manner, and apoptosis of Prx I knockdown MIN6 cells was increased by STZ stimulation, compared with untransduced MIN6 cells. Furthermore, an intraperitoneal injection of STZ increased pancreatic islet damage in Prx I knockout mice, compared with wildtype and Prx II knockout mice. AKT and glycogen synthase kinase (GSK)3ß phosphorylation significantly decreased following Prx I knockdown in MIN6 cells. However, phosphorylated ßcatenin and p65 levels significantly increased after STZ stimulation, compared with untransduced cells. The results of the present study indicate that deletion of Prx I mediated STZinduced pancreatic ßcell death in vivo and in vitro by regulating the AKT/GSK3ß/ßcatenin signaling pathway, as well as NFκB signaling. These findings provide a theoretical basis for treatment of pancreatic damage.
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Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Transducción de Señal
/
Regulación hacia Abajo
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Estreptozocina
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Diabetes Mellitus Experimental
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Células Secretoras de Insulina
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Peroxirredoxinas
Límite:
Animals
Idioma:
En
Año:
2020
Tipo del documento:
Article