hc-067047 and Brain-Injuries

Individuals with intracerebral hemorrhage (ICH) suffer varying degrees of neurological dysfunction as a result of neuronal apoptosis, and thus, maintenance of neuronal survival may be crucial to prevent ICH brain injury. Here, we report that the expression of transient receptor potential vanilloid 4 (TRPV4) was upregulated in mouse neurons after ICH. The selective TRPV4 agonist GSK1016790 A aggravated neuronal death whereas the TRPV4 antagonist HC-067047 promoted neuronal survival after ICH. We found that GSK1016790 A triggered Ca

Topics: Animals; Apoptosis; Brain Injuries; Calcium; Cell Death; Cell Survival; Cerebral Hemorrhage; Endoplasmic Reticulum Stress; Inositol 1,4,5-Trisphosphate Receptors; Leucine; Male; Mice; Mice, Inbred C57BL; Morpholines; Neurons; Pyrroles; Sulfonamides; TRPV Cation Channels; Unfolded Protein Response