Ontology highlight
ABSTRACT: Background and purpose
Inflammatory cells play a significant role in secondary injury after ischemic stroke. Recent studies have suggested that a lack of autophagy in myeloid cells causes augmented proinflammatory cytokine release and prolonged inflammation after tissue injury. In this study, we investigated the roles of myeloid cell autophagy in ischemic brain injury.Methods
Focal cerebral ischemia was induced via transient middle cerebral artery occlusion in mice with autophagy-deficient myeloid lineage cells (Atg5flox/flox LysMCre+) and in their littermate controls (Atg5flox/flox). Infarct volume, neurological function, inflammatory cell infiltration, and proinflammatory cytokine expression levels were evaluated.Results
Mice lacking autophagy in myeloid lineage c
SUBMITTER: Kotoda M
PROVIDER: S-EPMC5970995 | biostudies-literature | 2018 Jun
REPOSITORIES: biostudies-literature