Fig. 10.

Hyperosmolality-induced expression of Akr1b3 (aldose reductase) mRNA is affected by activation or expression of TRPM3. mIMCD-3 cells in which Trpm3 was deleted by CRISPR/Cas9 genome editing [TRPM3 knockout (KO)], as well as wild-type (WT) mIMCD-3 cells, were treated for 16 h with 0.1% DMSO or a TRPM3 agonist [100 μM pregnenolone sulfate (PSS)] at 300 mOsm/kg or 500 mOsm/kg [adjusted with NaCl (N)]. RT-qPCR was performed to determine mRNA expression relative to the reference gene B2m. Hyperosmolal stress induced Akr1b3 expression in both cell lines, but the response was greater in WT than TRPM3 KO cells. The TRPM3 agonist attenuated hyperosmolality-induced Akr1b3 expression in WT, but not TRPM3 KO, cells. %Significantly different (P < 0.05, by Student-Newman-Keuls method) from all other conditions. &Significantly different from all conditions except each other. No other comparisons were significantly different. n = 5 experiments.