S1P₂ contributes to microglial activation and M1 polarization following cerebral ischemia through ERK1/2 and JNK.

ABSTRACT: Sphingosine 1-phosphate (S1P) signaling has emerged as a drug target in cerebral ischemia. Among S1P receptors, S1P₂ was recently identified to mediate ischemic brain injury. But, pathogenic mechanisms are not fully identified, particularly in view of microglial activation, a core pathogenesis in cerebral ischemia. Here, we addressed whether microglial activation is the pathogenesis of S1P₂-mediated brain injury in mice challenged with transient middle cerebral artery occlusion (tMCAO). To suppress S1P₂ activity, its specific antagonist, JTE013 was given orally to mice immediately after reperfusion. JTE013 administration reduced the number of activated microglia and reversed their morphology from amoeboid to ramified microglia in post-ischemic brain after t

SUBMITTER: Sapkota A 

PROVIDER: S-EPMC6702157 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature