Effects of Trem2 depletion on gene expressions in a mouse photothrombotic stroke model
Ischemic stroke is a major threat to public health. Microglia-mediated neuroinflammation is a double-edged sword for neuronal survival after stroke. Triggering receptor expressed on myeloid cells 2 (Trem2) is specifically expressed on the surface of myeloid cell, including microglia. Here, we applied a photothrombotic mouse model of stroke to better understand the role of Trem2 in post-stroke neuroinflammation. In this model, Trem2 was sufficiently induced with sustainably elevated inflammatory responses. Our results demonstrated that Trem2-depletion can ameliorate ischemic injury with enhanced neuronal survival, reduced pro-inflammatory cytokine levels, and improved neurological functions. Our results suggested that Trem2 depletion is neuroprotective during ischemic stroke. Overall design: Photothromobotic stroke was induced in adult Trem2 wildtype (WT) or knockout (KO) mice by intraperitoneally injecting 50 mg/kg Rose Bengal followed by illumination with a 125 mW laser (525 nm wavelength) in specific cortical area. All the mice were male, 8-10 weeks old, with a C57Bl6 background. The cortical lesion region was restricted to a 3 mm-diameter circle centered approximately 2 mm lateral and -1 mm rostral to the bregma.The animals were perfused at 7 days post-injury (DPI), and their brains were stained with TTC for the precise isolation of infarction core (I), peri-infarction zone (P) and contralateral site (C).