TRPC6-Mediated Ca2+ Entry Essential for the Regulation of Nano-ZnO Induced Autophagy in SH-SY5Y Cells

Zhaowei Liu, Zhanqiang Du, Kai Li, Yangguang Han, Guogang Ren, Zhuo Yang

Research output: Contribution to journalArticlepeer-review


Recently, possible applications of zinc oxide nanoparticles (nano-ZnO) have been extensively studied owing to their ease of synthesis. However, the effect of nano-ZnO on the nervous system remains unclear. This study investigates the action of nano-ZnO on SH-SY5Y neuroblastoma cells. We found that nano-ZnO (0-50 µg/mL) induced a significant decrease in cell survival rate in a dose-dependent manner, and increased LC3 puncta formation. However, the apoptosis was not affected by nano-ZnO, because the protein levels of cytochrome c, caspase-3, Bcl-xL, and BAX were not varied by the nano-ZnO treatment. Nano-ZnO increased Ca2+ entry and the expression of TRPC6.The results suggested that nano-ZnO increased [Ca2+] through the TRPC-dependent Ca2+ influx, since Ca2+ influx can be prevented by the TRPC inhibitor. Furthermore, cells on nano-ZnO-treatment groups displayed loss of F-actin in a dose dependent manner, which also could be prevented by TRPC inhibitor. Herein, we demonstrated that the nano-ZnO activated TRPC6 channel, thereby increasing the Ca2+ flux and resulting in increased autophagy. Nano-ZnO could have possible anticancer effects in neuroblastoma by inhibiting the proliferation of tumor cells. However, we should also pay attention toward the biosecurity of nano materials.
Original languageEnglish
Pages (from-to)1602-1613
Number of pages12
JournalNeurochemical research
Early online date9 Apr 2020
Publication statusPublished - 1 Jul 2020


  • Autophagy
  • Ca
  • Current
  • Nano-ZnO
  • TRPC6


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