Lnc001209 Participates in aluminium-induced apoptosis of PC12 cells by regulating PI3K-AKT-mTOR signalling pathway

Abstract

Aluminium (Al) is a common environmental neurotoxin, but the molecular mechanism underlying its toxic effects remains unclear. Many studies have shown that aluminium exposure leads to increased neuronal apoptosis. This study aimed to investigate the mechanisms and signalling pathways involved in aluminium exposure-induced neuronal apoptosis. The results showed a decrease in the number of PC12 cells and changes in cell morphology in the aluminium maltol exposure group. The viability of PC12 cells decreased gradually with increasing of exposure doses, and the apoptosis rate increased. The expression of Lnc001209 decreased gradually with an increase in the aluminium exposure dose. After transfection of Lnc001209 siRNA in aluminium-exposed PC12 cells, the protein expression levels of p-Akt Ser473, p-Akt Thr308, p-P85 Tyr467, p-mTOR Ser2448 and CD36 were increased. RNA pull-down MS showed that Lnc001209 interacts with the CD36 protein. Expression of the CD36 protein was increased in PC12 cells exposed to aluminium. The results of the CD36 intervention experiment showed that the protein expression levels of p-Akt Ser473, p-Akt Thr308, p-P85 Tyr467, and p-mTOR Ser2448 likely increased after CD36 overexpression. In addition, the phosphorylation level of AKT had the most significant increase. The enhancement of p-Akt activity promotes neuronal apoptosis.

Keywords

• Aluminium
• Neuronal apoptosis
• Epigenetic modification
• Platelet glycoprotein 4 (Cluster of Differentiation 36, CD36)