PMID- 9987068
OWN - NLM
STAT- MEDLINE
DCOM- 19990415
LR  - 20131121
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 55
IP  - 2
DP  - 1999 Feb
TI  - Cyclooxygenase metabolites mediate glomerular monocyte chemoattractant protein-1 
      formation and monocyte recruitment in experimental glomerulonephritis.
PG  - 430-41
AB  - BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1) has been shown to play a 
      significant role in the recruitment of monocytes/macrophages in experimental 
      glomerulonephritis. Whereas a number of inflammatory mediators have been 
      characterized that are involved in the expression of MCP-1 in renal disease, 
      little is known about repressors of chemokine formation in vivo. We hypothesized 
      that cyclooxygenase (COX) products influence the formation of MCP-1 and affect 
      inflammatory cell recruitment in glomerulonephritis. METHODS: The effect of COX 
      inhibitors was evaluated in the antithymocyte antibody model and an 
      anti-glomerular basement membrane model of glomerulonephritis. Rats were treated 
      with the COX-1/COX-2 inhibitor indomethacin and the selective COX-2 inhibitors 
      meloxicam and SC 58125. Animals were studied at 1 hour, 24 hours, and 5 days 
      after induction of the disease. RESULTS: Indomethacin, to a lesser degree the 
      selective COX-2 inhibitors, enhanced glomerular MCP-1 and RANTES mRNA levels. 
      Indomethacin enhanced glomerular monocyte chemoattractant activity an the 
      infiltration of monocytes/macrophages at 24 hours and 5 days. CONCLUSIONS: Our 
      studies demonstrate that COX products may serve as endogenous repressors of MCP-1 
      formation in experimental glomerulonephritis. The data suggest that COX-1 and 
      COX-2 products mediate these effects differently because the selective COX-2 
      inhibitors had less influence on chemokine expression.
FAU - Schneider, A
AU  - Schneider A
AD  - Department of Medicine, University of Hamburg, Germany.
FAU - Harendza, S
AU  - Harendza S
FAU - Zahner, G
AU  - Zahner G
FAU - Jocks, T
AU  - Jocks T
FAU - Wenzel, U
AU  - Wenzel U
FAU - Wolf, G
AU  - Wolf G
FAU - Thaiss, F
AU  - Thaiss F
FAU - Helmchen, U
AU  - Helmchen U
FAU - Stahl, R A
AU  - Stahl RA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Chemokine CCL2)
RN  - 0 (Isoenzymes)
RN  - 0 (Membrane Proteins)
RN  - EC 1.14.99.1 (Cyclooxygenase 1)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases)
RN  - EC 1.14.99.1 (Ptgs1 protein, rat)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
CIN - Kidney Int. 1999 Feb;55(2):738-9. PMID: 9987099
MH  - Animals
MH  - Blotting, Northern
MH  - Blotting, Western
MH  - Cell Movement/physiology
MH  - Chemokine CCL2/*biosynthesis
MH  - Cyclooxygenase 1
MH  - Cyclooxygenase 2
MH  - Dinoprostone/biosynthesis
MH  - Glomerulonephritis/*metabolism/pathology/*physiopathology
MH  - Isoenzymes/metabolism
MH  - Kidney/pathology
MH  - Kidney Glomerulus/*metabolism
MH  - Male
MH  - Membrane Proteins
MH  - Monocytes/*physiology
MH  - Prostaglandin-Endoperoxide Synthases/*metabolism
MH  - Rats
MH  - Rats, Wistar
EDAT- 1999/02/13 00:00
MHDA- 1999/02/13 00:01
CRDT- 1999/02/13 00:00
PHST- 1999/02/13 00:00 [pubmed]
PHST- 1999/02/13 00:01 [medline]
PHST- 1999/02/13 00:00 [entrez]
AID - S0085-2538(15)45988-5 [pii]
AID - 10.1046/j.1523-1755.1999.00265.x [doi]
PST - ppublish
SO  - Kidney Int. 1999 Feb;55(2):430-41. doi: 10.1046/j.1523-1755.1999.00265.x.