Reduction of Diabetes-Induced Oxidative Stress, Fibrotic Cytokine Expression, and Renal Dysfunction in Protein Kinase Cβ–Null Mice

Reduction of Diabetes-Induced Oxidative Stress, Fibrotic Cytokine Expression, and Renal Dysfunction in Protein Kinase Cβ–Null Mice Yuzuru Ohshiro 1 , Ronald C. Ma 1 , Yutaka Yasuda 1 , Junko Hiraoka-Yamamoto 1 , Allen C. Clermont 1 , Keiji Isshiki 1 , Kunimasa Yagi 1 , Emi Arikawa 1 , Timothy S. Kern 2 and George L. King 1 1 Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts 2 Department of Medicine, Case Western Reserve University, Cleveland, Ohio Address correspondence and reprint requests to George L. King, Research Director, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215. E-mail: george.king{at}joslin.harvard.edu Abstract Diabetes induces the activation of several protein kinase C (PKC) isoforms in the renal glomeruli. We used PKC-β −/− mice to examine the action of PKC-β isoforms in diabetes-induced oxidative stress and renal injury at 8 and 24 weeks of disease. Diabetes increased PKC activity in renal cortex of wild-type mice and was significantly reduced (