Expressions of Wnt2 and β-catenin in Doxorubicin-induced myocardial injury and their relationships with p53 / 中华实用儿科临床杂志
Chinese Journal of Applied Clinical Pediatrics
;
(24): 370-373, 2015.
Article
in Chinese
| WPRIM
| ID: wpr-466825
ABSTRACT
Objective To investigate the expressions of Wnt2 and β-catenin in Doxorubicin (DOX)-induced myocardial injury and to explore their roles in myocardial cell apoptosis.Methods Cardiomyoblast cells were damaged by different concentrations of DOX(1 mg/L,2 mg/L,3 mg/L,4 mg/L) for 72 h.The effect of different concentrations of DOX on cardiomyocyte growth curve was detected according to the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-h-tetrazolium bromide(MTT) assay.DOX(1 mg/L) was used to induce the model of cardiomyoblast cell injury.Cardiomyocytes were divided into 4 groupsgroup ADOX-injured cardiomyocytes for 12 h ;group BDOX-injured cardiomyocytes for 24 h ; group CDOX-injured cardiomyocytes for 48 h; group Dnormal cardiomyocytes.The expressions of Wnt2,β-catenin and p53 were observed by Western blot and reverse transcription polymerase chain reaction(RT-PCR) at the time point of 12 h,24 h and 48 h.Results DOX significantly inhibited cardiomyocyte proliferation in a dose dependent fashion.The protein and mRNA expressions of Wnt2 increased in the DOX-induced myocardial injury group compared with the group D,with statistical significance (F =224.115,P < 0.05) ;The expressions of β-catenin,p53 were significantly increased compared with the group D,and the higher expression appeared with the time extending(F =188.145,231.927,all P < 0.05).Significantly positive correlation between Wnt2 and β-catenin expression was observed(r =0.940,P < 0.05).Conclusions These findings suggest that Wnt2/β-catenin signaling pathway may play important roles in the cardiovascular disease and be useful for exploring the molecular mechanism of myocardial injury..
Full text:
Available
Index:
WPRIM (Western Pacific)
Type of study:
Prognostic study
Language:
Chinese
Journal:
Chinese Journal of Applied Clinical Pediatrics
Year:
2015
Type:
Article
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