Results
Title

Necroptosis and microglia activation after chronic ischemic brain injury in mice.

Authors

Zhang, Shehong; Wang, Yuyang; Xie, Hongyu; Yu, Qing; Wu, Junfa; Wu, Yi; Zhu, Yulian

Abstract

Microglia, which are the resident macrophages and the first line of defense in the brain, can be activated within hours and migrate toward the injury sites after acute and chronic ischemic brain injury. However, a few studies have reported the interaction between microglia activation and necroptosis signaling following ischemic damage to the brain. In this study, chronic ischemic brain injury was induced by bilateral carotid artery stenosis (BCAS) and mice were sacrificed at 30 days after surgery. Ionized calcium-binding adaptor molecule 1 (IBA1) and glial fibrillary acidic protein (GFAP) immunostaining were performed to determine glial cell activation and inflammatory response. Tumor necrosis factor-α (TNF-α), interferon-γ (INF-γ), and interleukin-1β (IL-1β) proteins from the brains were examined to confirm inflammatory cytokines after BCAS. RIP1 and RIP3 proteins were detected to determine necroptosis signaling by Western blot. The data suggested that inflammatory responses, microglia activation, and necroptosis signaling are features of brain tissue pathology following BCAS-induced chronic ischemic brain injury.

Subjects

MICROGLIA; BRAIN injuries; CAROTID artery stenosis; IMMUNOSTAINING; NEUROGLIA; TUMOR necrosis factors; ISCHEMIA

Publication

European Journal of Inflammation, 2017, Vol 15, Issue 2, p78

ISSN

1721-727X

Publication type

Academic Journal

DOI

10.1177/1721727X17706855