c-Jun N-terminal kinase-mediated AP-1 activation in experimental glomerulonephritis in rats.
We demonstrated activation of transcription factor AP-1 in rat nephrotoxic 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. Increased JNKs activity was detected in glomeruli isolated from NTS-treated rats. The kinetics of JNKs activation was similar to that of AP-1 activation. Phosphorylated c-Jun at Ser63, one of the target residues for JNK, was also detected in nephritic glomeruli. This is the first report demonstrating JNKs-mediated c-Jun/AP-1 activation in nephritic glomeruli. These results suggest an important role of the JNK-AP-1 signaling pathway in the pathogenesis of glomerulonephritis.
Lead Generation Research Laboratory, Tanabe Seiyaku Co., Ltd., Osaka, Japan.
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Sakurai
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Sugita
D000818:Animals; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000378:metabolism*; D004789:Enzyme Activation; D005921:Glomerulonephritis / Q000378:metabolism* / Q000473:pathology; D048031:JNK Mitogen-Activated Protein Kinases; D007678:Kidney Glomerulus / Q000378:metabolism* / Q000473:pathology; D008297:Male; D020928:Mitogen-Activated Protein Kinases; D010766:Phosphorylation; D016755:Proto-Oncogene Proteins c-jun / Q000378:metabolism*; D051381:Rats; D011921:Rats, Inbred WKY; D015398:Signal Transduction; D018808:Transcription Factor AP-1 / Q000378:metabolism*
D016755:Proto-Oncogene Proteins c-jun; D018808:Transcription Factor AP-1; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D048031:JNK Mitogen-Activated Protein Kinases; D020928:Mitogen-Activated Protein Kinases