Over-activation of TRPM2 ion channel accelerates blood-spinal cord barrier destruction in diabetes combined with spinal cord injury rat
Susu Zhang, Jiaxin Zhao, Man Wu, Yongxiu Zhou, Xuejuan Wu, Anyu Du, Yibing Tao, Shanshan Huang, Shufang Cai, Mei Zhou, Tao Wei, Yanren Zhang, Ling Xie, Yanqing Wu, Jian Xiao
Abstract
influx and subsequently activated p-CaMKII/eNOS pathway, and which in turn triggered the ROS production. Consequently, over-activation of TRPM2 ion channel results in excessive apoptosis and weaker angiogenesis during SCI recovery. Inhibition of TRPM2 with 2-Aminoethyl diphenylborinate (2-APB) or TRPM2 siRNA will ameliorate the apoptosis of ECs and promote angiogenesis, subsequently enhance BSCB integrity and improve the locomotor function recovery of diabetes combined with SCI rat. In conclusion, TRPM2 channel may be a key target for the treatment of diabetes combined with SCI rat.