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. 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).