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Fig. 1 — C1q propagates microglial activation and neurodegeneration in the visual axis fo
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Created: 2026-04-21T18:29:40
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Fig. 1Figure 1
Retinal I/R injury significantly increases C1q expression in the retina. C57BL/6 J mice were subjected to unilateral I/R injury and sacrificed at the indicated time points post I/R. Contralateral control eyes ( a ) displayed basal deposits of C1q in the GCL; however, ischemic eyes ( b – f ) had significantly greater expression of C1q as early as day 3 ( b ) and sustained to the end of the time course on day 28 ( f ). Positive labeling was only observed in the GCL and IPL. ( g ) Fluorescence intensity quantification revealed statistically significant upregulation of C1q ( p < 0.01) at all time points in ischemic versus uninjured retinas. Peak intensity in ischemic eyes was observed on day 21 post injury ( p < 0.05). Mean ± SEM, n = 7 per group. ** p < 0.01 determined by student’s paired t -test, # p < 0.05 tested using One-way ANOVA followed by Holm-Sidak post test. GCL = Ganglion Cell Layer, INL = Inner Nuclear Layer, ONL = Outer Nuclear Layer. Scale bars = 50 μm
▸Metadata
| pmid | paper-828b7c4fa9a6 |
| caption | Retinal I/R injury significantly increases C1q expression in the retina. C57BL/6 J mice were subjected to unilateral I/R injury and sacrificed at the indicated time points post I/R. Contralateral cont |
| image_url | https://www.ebi.ac.uk/europepmc/articles/PMC4806521/bin/13024_2016_89_Fig1_HTML.jpg |
| paper_title | C1q propagates microglial activation and neurodegeneration in the visual axis following retinal ischemia/reperfusion injury. |
| figure_label | Fig. 1 |
| figure_number | 1 |
| _schema_version | 1 |
| source_strategy | pmc_api |
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