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Erratum for Kelly et al., J Am Soc Nephrol 14 (1) 128-138.
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J Am Soc Nephrol 14:823-824, 2003
© 2003 American Society of Nephrology

ERRATUM

In "P53 Mediates the Apoptotic Response to GTP Depletion after Renal Ischemia-Reperfusion: Protective Role of a p53 Inhibitor" by Kelly et al., which appeared in the January 2003 issue of JASN, Figures 8 and 9 were erroneously printed in black and white. They are printed below in color.



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  		Figure 8. Effect of antimycin/recovery and treatment with the p53 inhibitor PIF or guanosine (G) on apoptosis in cultured renal tubular cells. A representative fluorescent micrograph of LLC-PK1 cells demonstrating normal nuclear morphology is shown in panel A. Condensed, fragmented nuclei characteristic of apoptosis are seen after antimycin/recovery (0.1 µM antimycin A for 45 min and 24 h recovery; panel B). Apoptosis was not apparent in the cells treated with PIF (10 µM) before antimycin/recovery, as shown by the normal nuclear morphology in panel C. PIF alone did not alter nuclear morphology (panel D). Apoptosis after antimycin/recovery was also evident by characteristic laddering on DNA gel electrophoresis (panel E). Prevention of laddering was seen after antimycin/recovery in the presence of PIF (1 or 10 µM) or guanosine (G; 50 µM; panel E). m, DNA size markers.

 



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  		Figure 9. Effects of antimycin/recovery and PIF on the cellular localization of p53 in cultured renal tubular cells. Cultured LLC-PK1 renal tubular epithelial cells were harvested 24 h after exposure to antimycin A (0.1 µM for 45 min) with or without pifithrin-{alpha} (PIF; 10 µM) as detailed in Materials and Methods. Cells were fixed and immunostained with antibodies to p53 (Texas red-label, red) and the mitochondrial marker cytochrome c oxidase (FITC-label, green). Nuclei were stained with To-Pro-3 iodide (blue). Control cells were maintained in standard media.

 




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