Fig. 4: Altered lipid metabolism in L-ORD-iRPE contributes to reduced neuroprotective signaling.
From: AMPK modulation ameliorates dominant disease phenotypes of CTRP5 variant in retinal degeneration
a, b PEDF-R (red) immunolabeling in healthy-iRPE and L-ORD-iRPE. Cell nuclei (blue) and the actin cytoskeleton (phalloidin, green). Healthy-iRPE (n = 8), L-ORD-iRPE (n = 6). Scale bar: 10 µm. c Apical/basal ratio of PEDF secretion in L-ORD-iRPE (n = 11) as compared to healthy-iRPE (n = 12), measured by ELISA. d Phospholipase A2 activity in L-ORD-iRPE (n = 6) and healthy-iRPE (n = 5), measured by ELISA. e Phospholipase A2 activity of healthy-iRPE under basal and serum-starved (24 h) cell culture conditions (n = 6). f Seahorse assay results demonstrating oxygen consumption rate (OCR) in healthy (n = 18) and L-ORD-iRPE (n = 18) before and after the addition of mitochondrial respiration inhibitors (oligomycin, FCCP, antimycin A/rotenone). g ATP production measured from the Seahorse experiment in L-ORD-iRPE (21.4 ± 2.2 pmol/min, n = 18) compared to healthy-iRPE (58.7 ± 16.1 pmol/min, n = 18). h Apically secreted Neuroprotectin D1 (NPD1) measured by tandem mass spectrometry lipidomic analysis in POS-fed (4 h) L-ORD-iRPE (n = 12) and healthy-iRPE (n = 12). i Flow cytometry-based analysis of photoreceptor outer segment phagocytosis in L-ORD-iRPE and healthy-iRPE (n = 14). ∗p < 0.05, ∗∗p < 0.01.
