PMID- 11318946
OWN - NLM
STAT- MEDLINE
DCOM- 20010726
LR  - 20220311
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 59
IP  - 5
DP  - 2001 May
TI  - Monocyte chemoattractant protein-1 and osteopontin differentially regulate 
      monocytes recruitment in experimental glomerulonephritis.
PG  - 1762-9
AB  - BACKGROUND: This study evaluated the mechanisms of monocyte/macrophage (M/M) 
      infiltration in a rat model of anti-glomerular basement membrane 
      glomerulonephritis (GN). We focused on chemokines and osteopontin, which are 
      known regulators of M/M recruitment. METHODS: Using immunohistology, in situ 
      hybridization, and Northern blotting, the expression levels of chemokines and 
      osteopontin were evaluated in isolated glomeruli and tubules 4, 10, and 20 days 
      after the induction of GN. In vivo blocking experiments were performed by 
      application of neutralizing antibodies against osteopontin and monocyte 
      chemoattractant protein-1 (MCP-1). RESULTS: In nephritic animals, high glomerular 
      MCP-1 and RANTES (regulated upon activation normal T cell expressed and secreted) 
      expression levels were observed on days 4 and 10. The tubular expression of 
      MCP-1, however, was only slightly enhanced. In contrast, tubular osteopontin 
      production was maximally stimulated (day 10) and paralleled with peaks of 
      albuminuria and tubulointerstitial M/M infiltration. Application of an 
      anti-osteopontin antibody ameliorated tubulointerstitial and glomerular M/M 
      recruitment, whereas treatment with an anti-MCP-1 antibody selectively reduced 
      glomerular M/M recruitment. However, tubulointerstitial M/M infiltration remained 
      unchanged. CONCLUSION: These studies show that chemokines and osteopontin are 
      differentially expressed in glomeruli and tubules in this model of GN. Chemokines 
      play a primary role in the glomeruli, whereas osteopontin has a predominant role 
      in tubulointerstitial M/M recruitment. The roles of chemokines and osteopontin 
      may thus be dependent on the renal compartment and on the disease model.
FAU - Panzer, U
AU  - Panzer U
AD  - Department of Medicine, Division of Nephrology, University of Hamburg, Hamburg, 
      Germany.
FAU - Thaiss, F
AU  - Thaiss F
FAU - Zahner, G
AU  - Zahner G
FAU - Barth, P
AU  - Barth P
FAU - Reszka, M
AU  - Reszka M
FAU - Reinking, R R
AU  - Reinking RR
FAU - Wolf, G
AU  - Wolf G
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 (Chemokine CCL5)
RN  - 0 (Sialoglycoproteins)
RN  - 0 (Spp1 protein, rat)
RN  - 106441-73-0 (Osteopontin)
SB  - IM
MH  - Albuminuria/etiology
MH  - Animals
MH  - Basement Membrane/immunology
MH  - Cell Movement
MH  - Chemokine CCL2/antagonists & inhibitors/genetics/*physiology
MH  - Chemokine CCL5/genetics/metabolism
MH  - Disease Models, Animal
MH  - Gene Expression
MH  - Glomerulonephritis/etiology/*pathology/*physiopathology
MH  - Immunohistochemistry
MH  - In Situ Hybridization
MH  - Kidney Glomerulus/immunology
MH  - Macrophages/pathology/physiology
MH  - Male
MH  - Monocytes/pathology/*physiology
MH  - Neutralization Tests
MH  - Osteopontin
MH  - Rats
MH  - Rats, Wistar
MH  - Sialoglycoproteins/antagonists & inhibitors/genetics/*physiology
EDAT- 2001/04/25 10:00
MHDA- 2001/07/28 10:01
CRDT- 2001/04/25 10:00
PHST- 2001/04/25 10:00 [pubmed]
PHST- 2001/07/28 10:01 [medline]
PHST- 2001/04/25 10:00 [entrez]
AID - S0085-2538(15)47664-1 [pii]
AID - 10.1046/j.1523-1755.2001.0590051762.x [doi]
PST - ppublish
SO  - Kidney Int. 2001 May;59(5):1762-9. doi: 10.1046/j.1523-1755.2001.0590051762.x.