Alteration in Intracellular Zn²⁺ Homeostasis as a Result of TRPM2 Channel Activation Contributes to ROS-Induced Hippocampal Neuronal Death.

ABSTRACT: Transient receptor potential melastatin-related 2 (TRPM2) channel, a molecular sensor for reactive oxygen species (ROS), plays an important role in cognitive dysfunction associated with post-ischemia brain damage thought to result from ROS-induced TRPM2-dependent neuronal death during reperfusion. Emerging evidence further suggests that an alteration in the Zn²⁺ homeostasis is critical in ROS-induced TRPM2-dependent neuronal death. Here we applied genetic and pharmacological interventions to define the role of TRPM2 channel in ROS-induced neuronal death and explore the mechanisms contributing in the alteration in intracellular Zn²⁺ homeostasis in mouse hippocampal neurons. Exposure of neurons to 30-300 μM H₂O₂ for 2-24 h caused concentration/dura

SUBMITTER: Li X 

PROVIDER: S-EPMC5732979 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature