Microglial-specific depletion of TAK1 is neuroprotective in the acute phase after ischemic stroke.

ABSTRACT: Transforming growth factor-β-activated kinase 1 (TAK1) is upregulated after cerebral ischemia and contributes to an aggravation of brain injury. TAK1 acts as a key regulator of NF-ΚB and the MAP kinases JNK and p38 and modulates post-ischemic neuroinflammation and apoptosis. Microglia are the main TAK1-expressing immunocompetent cells of the brain. However, little is known about the function and regulation of microglial TAK1 after cerebral ischemia. Tamoxifen-dependent conditional depletion of TAK1 in microglial cells was induced in Cx3cr1^creER-Tak1^fl/fl mice. The cre^ER-negative Tak1^fl/fl mice and vehicle-treated (corn oil) mice served as control groups. A transient intraluminal middle cerebral artery occlusion of 30 min followed by 6 h and 72 h

SUBMITTER: Zeyen T 

PROVIDER: S-EPMC7297861 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature