AI Article Synopsis
- Animal models are crucial for studying podocytopathy and chronic kidney diseases (CKD), with Adriamycin (ADR)-induced nephropathy being a key rodent model.
- BALB/c mice are sensitive to ADR, whereas the commonly used C57BL/6 (B6) mice are resistant, necessitating the creation of a B6 strain that can develop ADR nephropathy.
- The study shows that the newly developed B6-Prkdc mutants progress to CKD after ADR treatment and reveals differences in gene expressions related to inflammation between B6-Prkdc and BALB/c mice, indicating a need for further research.
Article Abstract
Animal models of podocytopathy and chronic kidney diseases (CKD) help elucidate these pathologies. Adriamycin (ADR)-induced nephropathy is a common rodent model of podocytopathy. BALB/c mice are sensitive to ADR, whereas C57BL/6 (B6) mice, the most commonly used strain, are resistant to ADR. Therefore, mouse strains with the B6 genetic background cannot be used as an ADR nephropathy model. We previously generated DNA-dependent protein kinase catalytic subunit (Prkdc) mutant B6 mice (B6-Prkdc) carrying the R2140C mutation that causes ADR nephropathy. However, whether ADR nephropathy in the novel strain progresses to CKD after ADR administration has not been evaluated. Therefore, we examined whether the B6-Prkdc mice develop CKD after ADR administration. We also evaluated whether differences existed in the genetic background in ADR nephropathy by comparing the B6-Prkdc mice with BALB/c mice. Our findings demonstrated that B6-Prkdc progresses to CKD and is resistant to nephropathy compared with the BALB/c mice. The B6-Prkdc and BALB/c mice differed in the expression of genes related to inflammatory mediators, and further analysis is required to identify factors that contribute to resistance to nephropathy.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9978128 | PMC |
| http://dx.doi.org/10.1538/expanim.22-0057 | DOI Listing |
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