Evaluation of deoxynivalenol-induced toxic effects on mouse endometrial stromal cells: Cell apoptosis and cell cycle

Autor: Yinxue Xu, Yujian Dai, Haiqiang Xie
Rok vydání: 2017
Předmět:
G2 Phase
0301 basic medicine
Stromal cell
Cell Survival
MAP Kinase Signaling System
Cell
Poly (ADP-Ribose) Polymerase-1
Biophysics
Apoptosis
010501 environmental sciences
Biology
p38 Mitogen-Activated Protein Kinases
01 natural sciences
Biochemistry
Endometrium
Mice
03 medical and health sciences
Bcl-2-associated X protein
medicine
Animals
Viability assay
Cytotoxicity
Molecular Biology
Cells
Cultured
bcl-2-Associated X Protein
0105 earth and related environmental sciences
Cyclin-dependent kinase 1
Dose-Response Relationship
Drug
Caspase 3
Cell Cycle
Cell Biology
Cell cycle
Molecular biology
Caspase 9
Mitochondria
030104 developmental biology
medicine.anatomical_structure
Proto-Oncogene Proteins c-bcl-2
embryonic structures
biology.protein
Female
Stromal Cells
biological phenomena
cell phenomena
and immunity
Trichothecenes
Zdroj: Biochemical and Biophysical Research Communications. 483:572-577
ISSN: 0006-291X
DOI: 10.1016/j.bbrc.2016.12.103
Popis: Deoxynivalenol (DON) is a type B trichothecene mycotoxin which has toxic effects on humans and animals. Although DON has been studied in various cell types for its cytotoxicity, there is litter information about the effects of DON on mouse endometrial stromal cells (ESCs). Thus, in this study, we investigated the toxic effects of DON on mouse ESCs and its possible mechanisms. DON inhibited the cell viability in a dose- and time-dependent manner. TUNEL assay results showed that DON caused apoptosis and TUNEL-positive cells increased with increasing DON concentrations in mouse ESCs. Western blot showed that DON significantly increased the expression levels of apoptosis-related protein including Caspase-9, Caspase-3, poly (ADP-ribose) polymerase (PARP) and the ratio of Bax/Bcl-2. After DON treatment, the expression levels of cell cycle-related protein including p38/p-p38, Cdc25C/p-Cdc25C, Cdc2/p-Cdc2 and cyclinB1 were significantly decreased and immunoprecipitation analysis showed that cyclinB1-Cdc2 complex was significantly decreased. However, the combination of SB203580 (p38 specific inhibitor) and DON treatment significantly reversed the depression of Cdc25C/p-Cdc25C, Cdc2/p-Cdc2, cyclinB1 and cyclinB1-Cdc2 complex. Collectively, these data suggest that DON causes apoptosis via mitochondria apoptosis pathway and induces G2 arrest via p38 MAPK signaling pathway in mouse ESCs.
Databáze: OpenAIRE
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