Figure 1

Increased TNF-α and CCL2 production from microglia in retinal degeneration and NMDA-induced injury mice. (a and b) Retinae of rd1 and C57BL/6J control mice were used for flat-mount immunostaining at P14. Representative images showed that resting microglia in the control group featured with typical small cell bodies and long processes, and scarcely expressed TNF-α and CCL2. In contrast, the Iba-1⁺ microglia in rd1 mice assumed activated phenotypes, presented with enlarged somas and short lamellipodia. In addition, a strong co-labeling of TNF-α or CCL2 with Iba-1⁺ (white arrows) was observed in rd1 mice. (c and d) Adult C57BL/6J mice received a single intravitreal injection of NMDA to establish retinal neural injury, and vehicle (PBS) injection served as control. Retinae were harvested 24 h later for immunostaining. Similarly, Iba-1⁺ microglia in control mice exhibited resting statue, whereas microglia in NMDA-insult mice displayed activated morphology and expressed abundant TNF-α and CCL2. All images were acquired by confocal microscopy (Carl Zeiss LSM710). At least six mice were used per group. The right retina from each mouse was cut into four pieces equally and two images were captured randomly in each quarter of the retina. Scale bar: 50 μm