| First Author | Watanabe M | Year | 2021 |
| Journal | Biochem Biophys Res Commun | Volume | 556 |
| Pages | 121-126 | PubMed ID | 33839407 |
| Mgi Jnum | J:305297 | Mgi Id | MGI:6706018 |
| Doi | 10.1016/j.bbrc.2021.03.150 | Citation | Watanabe M, et al. (2021) A single amino acid substitution in PRKDC is a determinant of sensitivity to Adriamycin-induced renal injury in mouse. Biochem Biophys Res Commun 556:121-126 |
| abstractText | Adriamycin (ADR)-induced nephropathy is frequently utilized in rodent models of podocytopathy. However, the application of this model in mice is limited to a few strains, such as BALB/c mice. The most commonly used mouse strain, C57BL/6 (B6), is resistant to ADR-induced nephropathy, as are all mouse strains with a B6 genetic background. Reportedly, the R2140C variant of the Prkdc gene is the cause of susceptibility to ADR-induced nephropathy in mice. To verify this hypothesis, we produced Prkdc mutant B6 mice, termed B6-Prkdc(R2140C), that possess the R2140C mutation. After administration of ADR, B6-Prkdc(R2140C) mice exhibited massive proteinuria and glomerular and renal tubular injuries. In addition, there was no significant difference in the severity between B6-Prkdc(R2140C) and BALB/c. These findings demonstrated that B6-Prkdc(R2140C) show ADR-induced nephropathy susceptibility at a similar level to BALB/c, and that the PRKDC R2140C variant causes susceptibility to ADR-induced nephropathy. In future studies, ADR-induced nephropathy may become applicable to various kinds of genetically modified mice with a B6 background by mating with B6-Prkdc(R2140C). |
