Time‑course analysis of cisplatin induced AKI in preclinical models: implications for testing different sources of MSCs

Cisplatin remains the most effective and widely used treatment option for solid tumors, however, it is also responsible for 30 - 46% incidence of AKI in cancer patients. Thus, despite its broad anti-cancer potential, clinical use of this chemotherapeutic agent remains constrained. In the last decade, mesenchymal stem cells (MSCs) have been proposed as a potentially useful therapeutic strategy in various diseases, including AKI, given their ability to reduce apoptosis and accelerate tubular cell regeneration. In the present study, we looked at the dose dependent response to cisplatin in two different mouse strains, CD1 and C57BL/6 mice, and performed a transcriptome based time-series analysis of the molecular signature in both male and female mice during progression of cisplatin-induced AKI, in order to generate a robust and reproducible pre-clinical model with the proposed aim to investigate the ability of MSCs from three different sources (adult and neonatal) as a rescue therapy to reverse kidney injury.