Fig. 7

EPO silencing aggravated pronephros structure and function in hyperglycemic zebrafish. A. Further enlarged glomerulus (white arrow head) and shortened pronephric neck (white asterixis) in EPO + Pdx1 morphants (EPO + Pdx1 MO.) as compared to Pdx1 morphants (Pdx1 MO.) alone. White scale bar: 200 μm. B. Quantification of data in Figure A performed in three independent experiments. (n = 55–69 embryos per group). ***p < 0.001 as indicated. C. Elevated loss of 70 kDa dextran–FITC fluorescence at 24 hpi and 48 hpi in Pdx1 MO. as compared to Control MO. but decreased loss of 70 kDa dextran–FITC fluorescence at 24 hpi and 48 hpi in EPO + Pdx1 MO. as compared to Control MO. (n = 39–44 embryos per group). Significance was given for Pdx1 MO. against Control MO. as ***p < 0.001, and for EPO + Pdx1 MO. against Control MO. as ###p < 0.001. All data were analyzed using the Student‘s t-test. Mean ± s.e.m. D. Schematic illustration that EPO and EPOR maintain kidney structure and function through repressing apoptosis and protect kidney pathogenesis under hyperglycemia condition.