CDK4-pRB-E2F1 pathway may mediate A?_(1-40)-induced apoptosis in rat cortical neurons
- VernacularTitle:CDK4-pRB-E2F1通路是A?_(1-40)诱导皮层神经元凋亡的可能途径
- Author:
Limin CHEN
;
Xiaochun CHEN
;
Tingyan LIN
;
Yuangui ZHU
;
Chaohui ZHAO
;
Yican ZHOU
- Publication Type:Journal Article
- Keywords:
Amyloid beta-peptide;
CDK4-pRB-E2F1 pathway;
Apoptosis;
Neurons;
Rats
- From:
Chinese Journal of Pathophysiology
2000;0(08):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To study the possible molecular mechanism of beta-amyloid peptide_ 1-40 -induced apoptosis in rat cortical neurons. METHODS: 40 mg/L beta-amyloid peptide_ 1-40 (A?_ 1-40 ) was used to induce apoptosis in cultured rat cortical neurons. The level of CDK4, phosphorylated pRB were detected by flow cytometry and immunoblotting; RT-PCR was used to examine the mRNA expression of E2F1 while fluorescent spectrofluorometer was used to measure caspase-3 activity. All of the above study was designed to observe whether the level of CDK4, phosphorylated pRB and E2F1 mRNA expression could be affected by A?_ 1-40 . RESULTS: (1)The level of CDK4, phosphorylated pRB increased markedly 2-4 hours after treatment with A?_ 1-40 , and caspase-3 activity elevated remarkably 12-24 hours after treatment with A?_ 1-40 ; (2) E2F1 mRNA expression was upregulated 3 hours after incubation with A?_ 1-40 . CONCLUSION: A?_ 1-40 may induce apoptosis in rat cortical neurons in a manner dependent on CDK4-pRB-E2F1 pathway.
