Effects of lysophosphatidylcholine on β-amyloid-induced neuronal apoptosis

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Abstract
We have investigated the effects of lysophosphatidylcholine (LPC), a product of lipid peroxidation, on Aβ1–42-induced SH-SY5Y cell apoptosis. The viability of cultured SH-SY5Y cells was measured using a CCK-8 kit. Apoptosis was determined by Chip-based flow cytometric assay. The mRNA transcription of Bcl-2, Bax, and caspase-3 were detected by using reverse transcription and real-time quantitative PCR and the protein levels of Bax and caspase-3 were analyzed by Western blotting. The cytosolic calcium concentration of SH-SY5Y cells was tested by calcium influx assay. G2A expression in SH-SY5Y cells was silenced by small interfering RNA. Long-term exposure of SH-SY5Y cells to LPC augmented the neurotoxicity of Aβ1–42. Furthermore, after LPC treatment, the Bax/Bcl-xL ratio and the expression levels, as well as the activity of caspase-3 were, elevated, whereas the expression level of TRAF1 was reduced. Because LPC was reported to be a specific ligand for the orphan G-protein coupled receptor, G2A, we investigated LPC-mediated changes in calcium levels in SH-SY5Y cells. Our results demonstrated that LPC can enhance the Aβ1–42-induced elevation of intracellular calcium. Interestingly, Aβ1–42 significantly increased the expression of G2A in SH-SY5Y cells, whereas knockdown of G2A using siRNA reduced the effects of LPC on Aβ1–42-induced neurotoxicity. The effects of LPC on Aβ1–42-induced apoptosis may occur through the signal pathways of the orphan G-protein coupled receptor.

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