Aβ1-42 regulates astrocytes through JNK/AP-1 pathway

G.-Q. Li, D.-W. Cong, P. Sun, X. Meng

Neurology Intensive Care Unit, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. mengxu825@sina.com

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• Neurology

OBJECTIVE: In Alzheimer’s disease (AD), astrocytes are generally found in the surrounding of senile plaques participating in the production of phagocytosis and the removal of toxic compounds such as Aβ. This study aimed at investigating the effect of Aβ1-42 on astrocytes.

MATERIALS AND METHODS: Cellular viability of primary cultured astrocytes was analyzed using CCK-8 assay. Quantitative Real-time PCR was used to assess the mRNA expression of JNK and AP-1. The proteins of JNK/AP-1 pathway were investigated using Western blot.

RESULTS: Our findings showed that Aβ1-42 inhibited cell viability and promoted apoptosis in astrocytes in primary culture. Additionally, Aβ1-42 increased the mRNA expression level of AP-1, but had no effect on the expression of JNK. Furthermore, Aβ1-42 increased the protein expression of p-JNK, p-c-jun and Fra-1 and the ratio of p-c-jun/c-jun and p-JNK/JNK.

CONCLUSIONS: We showed that Aβ1-42 promoted cell apoptosis in astrocytes in primary culture. Furthermore, Aβ1-42 activated JNK/AP-1 pathway through promoting the phosphorylation of JNK, c-jun and Fra-1 expression, then inducing cell apoptosis.

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