Fig. 2: Binding of S1P by ApoM is necessary for RPE lipotoxicity amelioration. | Nature Communications

Fig. 2: Binding of S1P by ApoM is necessary for RPE lipotoxicity amelioration.

From: Apolipoprotein M attenuates age-related macular degeneration phenotypes via sphingosine-1-phosphate signaling and lysosomal lipid catabolism

Fig. 2

A High fat diet fed Abca1/g1-rod/-rod were treated with plasma from either control mice with human ApoM knocked in (ApoMCtrl) or mice expressing ApoM incapable of binding S1P (ApoMTM) (created in BioRender. Lee, T. (2025) https://BioRender.com/li4w1zf). Full-field scotopic electroretinography (n = 4) demonstrated significant reduction in B rod photoreceptor (*p = 0.0469, Two-way ANOVA) and C inner retina function (*p < 0.0199, Two-way ANOVA) in ApoMTM treated mice. D Representative traces of 0 dB intensity flashes show the waveform from ApoMTM treated mice do not recover. E, F Representative TEM imaging of RPE from either ApoMCtrl or ApoMTM plasma treated Abca1/g1-rod/-rod mice. Red arrows point to lipid droplets. G Quantitative assessment of lipid droplets per high-powered field within the RPE (n = 45) revealed significantly increased lipid droplets in ApoMTM plasma treated mice (****p < 0.000000013, two-tailed Welch’s t-test). H Quantitative assessment of melanosomes per high-powered field within the RPE (n = 45) revealed no significant difference according to two-tailed Welch’s t-test without multiple comparisons in melanosome counts between ApoMCtrl and ApoMTM plasma treated mice. Scale bar represents 2 μm. Values are mean ± SE. Source data are provided as a Source Data file.

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