- Masahiko Satoh (Laboratory of Pharmaceutical Health Sciences, School of Pharmacy, Aichi Gakuin University / firstname.lastname@example.org)
1) Laboratory of Pharmaceutical Health Sciences, School of Pharmacy, Aichi Gakuin University , 2) Department of Environmental Health, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences , 3) College of Pharmacy, Dongguk University, Korea
Cadmium (Cd) is a nephrotoxic heavy metal. Several signal transduction pathways have been reported to be associated with Cd toxicity. GPRC5B is a member of the family of G-protein-coupled receptors, which recognize various ligands and can transmit signals from the cell surface into the cell interior. We examined the involvement of GPRC5B in Cd toxicity in HK-2 human proximal tubular cells. Herein, we found that Cd significantly reduced GPRC5B gene expression in HK-2 cells. Moreover, knockdown of GPRC5B by siRNA transfection strengthened Cd toxicity in HK-2 cells. Our findings suggest that Cd partially conferred its toxicity by suppressing GPRC5B gene expression in HK-2 cells.