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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Exp Neurol. 2015 Feb 25;267:1–12. doi: 10.1016/j.expneurol.2015.02.027

Fig. 1.

Fig. 1

Reduced pro-Inflammatory chemokine and TNF-α transcript expression in the rd1 mouse in the absence of MyD88-mediated signaling. (A-F) Expression of Ccl2 (MCP-1), Ccl4 (MIP-1β), Ccl7 (MCP-3), Cxcl10, Ccl3 (MIP-1α), and Ccl5 (RANTES) in rd1/MyD88+/+ and rd1/MyD88-/- mice at postnatal day 12 (P12), P14 and P16, as measured by qPCR. Reduced transcript levels and a shift in the peak expression from P12 to P14 was observed in MyD88-/- compared with MyD88+/+, for Ccl4, Ccl5, Ccl7, and Cxcl10 (n=3-5, p<0.05). In contrast, Ccl5 expression level remains relatively constant as retinal degeneration progresses with a consistent 2-fold reduction in the rd1/MyD88-/- mouse (n=3-5, p<0.05), whereas Ccl3 expression was not different between the two genotypes. (G) Retinal expression of TNF-α is reduced by 4.4 fold in the rd1/MyD88-/- compared with rd1/MyD88+/+ at P12 (n=3 each, p<0.05). TNF-α expression was normalized to ARP and was expressed relative to expression in the BV2 microglial cell line due to lack of expression in WT retina. Mean ± SEM are shown. * p<0.05, comparison between genotypes within a given time-point p<0.05; (x0005E) p<0.05, comparison among ages of the same genotype; # p<0.05, comparison of peak expression between rd1/MyD88+/+ and rd1/MyD88-/-across all time-points. Samples were compared with the house-keeping gene acid ribosomal phosphoprotein (ARP). All samples were normalized to that of a wild type adult mouse retina, except for TNF-α, which was not detected in wild type retina, and was instead compared with the murine microglial cell line BV2.