The potassium channel KCa3.1 constitutes a pharmacological target for astrogliosis associated with ischemia stroke.

ABSTRACT:

Background

Reactive astrogliosis is one of the significantly pathological features in ischemic stroke accompanied with changes in gene expression, morphology, and proliferation. KCa3.1 was involved in TGF-β-induced astrogliosis in vitro and also contributed to astrogliosis-mediated neuroinflammation in neurodegeneration disease.

Methods

Wild type mice and KCa3.1^-/- mice were subjected to permanent middle cerebral artery occlusion (pMCAO) to evaluate the infarct areas by 2,3,5-triphenyltetrazolium hydrochloride staining and neurological deficit. KCa3.1 channels expression and cell localization in the brain of pMCAO mice model were measured by immunoblotting and immunostaining. Glia activation and neuron loss was measured by immunostaining. DiBAC4 (3) and Fluo-4AM w

SUBMITTER: Yi M 

PROVIDER: S-EPMC5644250 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature