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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: IL-33 deficiency causes persistent inflammation and severe neurodegeneration in retinal detachment

Fig. 2

RD results in an acute inflammatory response in WT retina. At different days following RD, the retinas were collected and processed for RT-PCR analysis of inflammatory genes in WT mice (a–f). The mRNA expression of CCL2 (a), C1ra (b), C1s (c), IL-1β (d) and IL-18 (e) at days 1, 4, 7, and 28 post-RD. f The expression level of TNFα peaked at day 4 and remained at the peak at day 7 and returned back to the basal level at day 28 post-RD. g The expression level of IL-33 peaked at day 1, then decreased towards the basal level at day 28 post-RD. h The expression level of GFAP peaked at day 1 and reduced gradually. At day 28 post-RD, the expression level of GFAP was maintained at a higher level than control. Data presented as mean ± SEM, n = 6 per group, one-way ANOVA followed by Dunnett’s multiple comparisons test, *P < 0.05, **P < 0.01, ***P < 0.001. i, j Representative images of retinal sections stained for glutamine synthetase (red, marker for Müller cells), IL-33 (green) and DAPI (blue) in i detached retina (day 28 post-RD) and j normal retina. IL-33 was localised in the nuclei of Müller cells, and no significant IL-33 signal (green) could be observed out of Müller cells in detached retina. Scale bar, 50 μm

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