Source:http://linkedlifedata.com/resource/pubmed/id/17597698
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
|
pubmed:dateCreated |
2007-9-6
|
pubmed:abstractText |
Activation of the c-Jun NH2-terminal kinase (JNK) signaling pathway is involved in the immune response; however, little is known of its role in immune-induced renal injury. In this study, we examine JNK signaling in the rat anti-glomerular basement membrane (GBM) disease model using CC-401, a specific JNK inhibitor. Animals were given CC-401, vehicle alone or no treatment starting before anti-GBM serum injection and continued treatment until killing. In acute disease, CC-401 blocked JNK signaling and reduced proteinuria in the first 24 h. The transient neutrophil influx seen at 3 h of disease was not affected, however. Continued CC-401 treatment suppressed glomerular and tubulointerstitial damage usually seen at 14 days. The protective effect may be due to modulation of macrophage activation, as CC-401 had no effect upon glomerular macrophage infiltration at day 14 despite the suppression of glomerular lesions and a marked reduction in renal tumor necrosis factor-alpha and inducible nitric oxide synthase messenger RNA levels. Treatment with CC-401 had no apparent effect on T cell or humoral immune responses. These studies suggest that JNK signaling promotes renal injury in acute and progressive rat anti-GBM disease. JNK inhibitors may be a novel therapeutic approach for the treatment of human glomerulonephritis.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Sep
|
pubmed:issn |
0085-2538
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
72
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
698-708
|
pubmed:dateRevised |
2009-11-19
|
pubmed:meshHeading |
pubmed-meshheading:17597698-Acute Disease,
pubmed-meshheading:17597698-Animals,
pubmed-meshheading:17597698-Anti-Glomerular Basement Membrane Disease,
pubmed-meshheading:17597698-Disease Models, Animal,
pubmed-meshheading:17597698-Enzyme Activation,
pubmed-meshheading:17597698-Enzyme Inhibitors,
pubmed-meshheading:17597698-JNK Mitogen-Activated Protein Kinases,
pubmed-meshheading:17597698-Kidney Glomerulus,
pubmed-meshheading:17597698-Macrophages,
pubmed-meshheading:17597698-Neutrophils,
pubmed-meshheading:17597698-Pyrazolones,
pubmed-meshheading:17597698-Rats,
pubmed-meshheading:17597698-Rats, Sprague-Dawley,
pubmed-meshheading:17597698-Signal Transduction,
pubmed-meshheading:17597698-T-Lymphocytes
|
pubmed:year |
2007
|
pubmed:articleTitle |
A pathogenic role for JNK signaling in experimental anti-GBM glomerulonephritis.
|
pubmed:affiliation |
Department of Nephrology, Monash Medical Centre, Clayton, Victoria, Australia.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|