Figure 5 | Scientific Reports

Figure 5

From: Characterizing renal involvement in Hermansky-Pudlak Syndrome in a zebrafish model

Figure 5

HPS1KD ATG, HPS3KD ATG, HPS4KD ATG and HPS5KD ATG induce varying degrees of glomerular damage including podocyte effacement and deposition of intracellular debris (zebra bodies). Transmission electron microscopy imaging was used to detect ultrastructural changes in glomeruli after HPS protein knockdown induced by MO injection in Tg(l-fabp:eGFP-DBP) transgene zebrafish embryos at a one to four cell stage. Collection of larvae for imaging was done at 120 hpf. (A) HPS1KD ATG causes loss of glomerular endothelial fenestration and podocyte effacement. HPS3KD ATG induces mild podocyte effacement. HPS4KD ATG causes podocyte effacement without endothelial injury, while HPS5KD ATG leads to reduced endothelial fenestration and podocyte effacement. Zebrafish injected with a control morpholino (CTRL-MO) show no sign of glomerular damage. Scale bar = 2 µm. (B) Induction of HPS protein knockdown of HPS1, -3, -4 and -5 leads to the deposition of intracellular debris primarily in podocytes. Scale bar = 500 nm.

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