| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Medicine, McGill University Health Centre, Montreal, Quebec, Canada H3A 2B4
First published July 12, 2001;
10.1152/ajprenal.0048.2001.
In rat membranous nephropathy,
complement C5b-9 induces glomerular epithelial cell (GEC) injury and
proteinuria, which is partially mediated by eicosanoids. Rat GEC in
culture express cyclooxygenase (COX)-1 constitutively, whereas COX-2
expression is induced by C5b-9. Both isoforms contribute to
complement-induced prostaglandin generation. The present study
addresses mechanisms of complement-induced COX-2 expression in GEC.
Downregulation of protein kinase C (PKC) blunted complement-induced
upregulation of COX-2 mRNA. Complement and phorbol 12-myristate
13-acetate (PMA) both stimulated COX-2 promoter activity. C5b-9
activated c-Jun NH2-terminal kinase (JNK), and inhibition
of JNK activity by transfection of a kinase-inactive JNK1 partially
inhibited complement-induced (but not PMA-induced) COX-2 promoter
activation. Conversely, a constitutively active mitogen-activated
protein or extracellular signal-regulated kinase kinase kinase
(MEKK)-1, a kinase upstream of JNK, increased COX-2 promoter activity.
MEKK-induced COX-2 promoter activation was not affected by
downregulation of PKC and was augmented by PMA. Thus, in GEC, PKC and
JNK pathways contribute independently to complement-induced COX-2
expression. Nuclear factor-
B was also activated by complement in GEC
but did not contribute to complement-induced COX-2 upregulation.
c-Jun NH2-terminal kinase; eicosanoid; lipid mediators; membranous nephropathy; signal transduction
This article has been cited by other articles:
|
|
 |
|
  J. Ke, X. Long, Y. Liu, Y.F. Zhang, J. Li, W. Fang, and Q.G. Meng Role of NF-{kappa}B in TNF-{alpha}-induced COX-2 Expression in Synovial Fibroblasts from Human TMJ Journal of Dental Research, April 1, 2007; 86(4): 363 - 367. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. V. Cybulsky Cyclooxygenases, Prostanoids, and Glomerular Injury: Complex Relationships J. Am. Soc. Nephrol., February 1, 2007; 18(2): 367 - 368. [Full Text] [PDF]
|
|
|
|
 |
|
 A. V. Cybulsky, R. J. Quigg, and D. J. Salant Experimental membranous nephropathy redux Am J Physiol Renal Physiol, October 1, 2005; 289(4): F660 - F671. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. T. Lappegard, J. Riesenfeld, O.-L. Brekke, G. Bergseth, J. D. Lambris, and T. E. Mollnes Differential Effect of Heparin Coating and Complement Inhibition on Artificial Surface-Induced Eicosanoid Production Ann. Thorac. Surg., March 1, 2005; 79(3): 917 - 923. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Aoudjit, M. Stanciu, H. Li, S. Lemay, and T. Takano p38 Mitogen-activated protein kinase protects glomerular epithelial cells from complement-mediated cell injury Am J Physiol Renal Physiol, October 1, 2003; 285(4): F765 - F774. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. I. Lemieux, S. S. Rahal, and C. R. J. Kennedy PGE2 reduces arachidonic acid release in murine podocytes: evidence for an autocrine feedback loop Am J Physiol Cell Physiol, February 1, 2003; 284(2): C302 - C309. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Peng, T. Takano, J. Papillon, K. Bijian, A. Khadir, and A. V. Cybulsky Complement Activates the c-Jun N-Terminal Kinase/Stress-Activated Protein Kinase in Glomerular Epithelial Cells J. Immunol., September 1, 2002; 169(5): 2594 - 2601. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
