Methotrexate treatment can restore nephrocyte function following a high-fat diet
Nephrocytes from control Drosophila (w1118; 7-day-old females) fed a regular diet (normal fat diet, NFD) or high-fat diet (NFD supplemented with 14% coconut oil, HFD), with or without methotrexate (10 μM; ex vivo 60 min) treatment. (A) Representative confocal images of FITC-albumin fluorescence (green). Scale bar: 50 μm. (B) Box plot shows the quantitation of the relative fluorescence intensity of FITC-albumin uptake based on images in (A); middle line depicts the median and whiskers show Tukey. Statistical analysis was performed by two-way ANOVA with Sidak correction; ****, P<0.0001; ns, not significant; n = 30 from six 1-day-old females (5 nephrocytes/fly). (C) Representative confocal images of 10 kD dextran fluorescence (red). Scale bar: 50 μm. (D) Box plot shows the quantitation of the relative fluorescence intensity of 10 kD dextran uptake based on images in (C); middle line depicts the median and whiskers show Tukey. Statistical analysis was performed by Mann-Whitney U test; ****, P<0.0001; ns, not significant; n = 30 from six 1-day-old females (5 nephrocytes/fly). (E) Graphic of proposed model for high-fat diet-induced nephrocyte defects via an adipose-nephrocyte axis. A high-fat diet upregulates the expression and secretion of the adipokine Unpaired 2 (Upd2), leptin-like hormone, from the fat body. Upd2 is a JAK-STAT ligand, and it activates JAK-STAT signaling at the nephrocytes (Signal-transducer and activator of transcription 92E, Stat92E; Suppressor of cytokine signaling at 36E, Socs36E; JAK Hopscotch, Hop; Domeless, Dome). The overactive JAK-STAT pathway disrupts the integrity of the slit diaphragm (SD) filtration structure and thereby leads to nephrocyte dysfunction.