Enhanced store-operated calcium entry (SOCE) exacerbates motor neurons apoptosis following spinal cord injury

Spinal cord injury is pathologically characterized by the loss of motor function caused neurons apoptosis. Store-operated calcium entry (SOCE) widely known to dictate apoptosis various cell types. To examine SOCE in spinal and explore role apoptosis, patients with (SCI) SCI mouse models were included. Expression components apoptosis-related proteins examined Western blotting. Calcium imaging was used assess activity. As a result, we confirmed enhanced levels ORAI1 STIM1 models. In vitro study, tunicamycin impaired viability VSC4.1 cells (motoneuron-neuroblastoma hybrid line) increased activity, effects which could be abolished 2-APB. Furthermore, tunicamycinreduced BCL-2/BAX ratio also reversed Additionally, EdU assay DCFH-DA staining regulatory 2-APB proliferation ROS production. Of note improved hindlimb alleviated depression administration. Therefore, conclude that may contribute pathogenesis exacerbating motoneurons.