C-JUN N-TERMINAL KINASE-MEDIATED AP-1 ACTIVATION IN EXPERIMENTAL GLOMERULONEPHRITIS IN RATS

We demonstrated activation of transcription factor AP-1 in rat nephrot oxlc serum (NTS)-induced glomerulonephritis in a previous report. Here , we evaluate c-Jun N-terminal kinases (JNKs) activity to clarify the molecular mechanisms of AP-1 activation in nephritic glomeruli. Increa sed JNKs activity was detected in glomeruli isolated from NTS-treated rats. The kinetics of JNKs activation was similar to that of AP-1 acti vation. Phosphorylated c-Jun at Ser(63), one of the target residues fo r JNK, was also detected in nephritic glomeruli. This is the first rep ort demonstrating JNKs-mediated c-Jun/AP-1 activation in nephritic glo meruli. These results suggest an important role of the JNK-AP-1 signal ing pathway in the pathogenesis of glomerulonephritis.