PMID- 11115074
OWN - NLM
STAT- MEDLINE
DCOM- 20010111
LR  - 20151119
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 58
IP  - 6
DP  - 2000 Dec
TI  - Monocyte chemoattractant protein-1 and macrophage infiltration in hypertensive 
      kidney injury.
PG  - 2408-19
AB  - BACKGROUND: We investigated whether monocyte chemoattractant protein-1 (MCP-1) is 
      expressed in hypertensive nephrosclerosis, and tested the effect of angiotensin 
      II type 1 receptor blockade on MCP-1 expression and macrophage (MPhi) 
      infiltration. METHODS: Rats with two-kidney, one-clip (2K1C) hypertension with 
      and without treatment with the angiotensin II type 1 receptor antagonist 
      valsartan (3 mg/kg/day) were studied. In these animals as well as in 
      spontaneously hypertensive rats (SHR), stroke-prone SHR (SHR-SP), hypertensive 
      mRen-2 transgenic rats (TGR), and respective control strains, MCP-1 expression in 
      the kidney was investigated by Northern and Western blots and by 
      immunohistochemistry. Glomerular and interstitial MPhis were counted. RESULTS: In 
      the nonclipped kidney of 2K1C rats, MCP-1 expression was elevated at 14 and 28 
      days when significant MPhi infiltration was present. MCP-1 was localized to 
      glomerular endothelial and epithelial cells, interstitial and tubular cells, 
      MPhis, and vascular smooth muscle cells. A similar pattern of MCP-1 staining was 
      present in TGR kidneys, whereas MCP-1 expression was not increased in SHR and 
      SHR-SP. Valsartan reduced but did not normalize blood pressure, blocked the 
      induction of MCP-1 protein in 2K1C kidneys, and decreased interstitial MPhi 
      infiltration significantly. CONCLUSION: MCP-1 expression is increased in 
      angiotensin II-dependent models of hypertensive nephrosclerosis and is temporally 
      and spatially related to MPhi infiltration. The angiotensin II type 1 receptor 
      mediates the induction of MCP-1.
FAU - Hilgers, K F
AU  - Hilgers KF
AD  - Department of Medicine IV, University of Erlangen-Nurnberg, Erlangen; 
      Max-Delbruck-Center, Berlin-Buch, Germany. karl.hilgers@rzmail.uni-erlangen.de
FAU - Hartner, A
AU  - Hartner A
FAU - Porst, M
AU  - Porst M
FAU - Mai, M
AU  - Mai M
FAU - Wittmann, M
AU  - Wittmann M
FAU - Hugo, C
AU  - Hugo C
FAU - Ganten, D
AU  - Ganten D
FAU - Geiger, H
AU  - Geiger H
FAU - Veelken, R
AU  - Veelken R
FAU - Mann, J F
AU  - Mann JF
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 (Angiotensin Receptor Antagonists)
RN  - 0 (Antihypertensive Agents)
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptor, Angiotensin, Type 1)
RN  - 0 (Receptor, Angiotensin, Type 2)
RN  - 0 (Receptors, Angiotensin)
RN  - 0 (Tetrazoles)
RN  - 80M03YXJ7I (Valsartan)
RN  - HG18B9YRS7 (Valine)
SB  - IM
MH  - Angiotensin Receptor Antagonists
MH  - Animals
MH  - Antihypertensive Agents/pharmacology
MH  - Blood Pressure
MH  - Chemokine CCL2/analysis/*genetics
MH  - Chemotaxis, Leukocyte/immunology
MH  - Gene Expression/physiology
MH  - Hypertension, Renal/drug therapy/*immunology/pathology
MH  - Kidney/chemistry/immunology/pathology
MH  - Kidney Failure, Chronic/immunology
MH  - Macrophages/cytology/*immunology
MH  - Monocytes/cytology/immunology
MH  - Nephrosclerosis/drug therapy/immunology/pathology
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Rats, Mutant Strains
MH  - Rats, Sprague-Dawley
MH  - Receptor, Angiotensin, Type 1
MH  - Receptor, Angiotensin, Type 2
MH  - Receptors, Angiotensin/physiology
MH  - Tetrazoles/pharmacology
MH  - Valine/*analogs & derivatives/pharmacology
MH  - Valsartan
EDAT- 2000/12/15 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/12/15 11:00
PHST- 2000/12/15 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/12/15 11:00 [entrez]
AID - S0085-2538(15)47357-0 [pii]
AID - 10.1046/j.1523-1755.2000.00424.x [doi]
PST - ppublish
SO  - Kidney Int. 2000 Dec;58(6):2408-19. doi: 10.1046/j.1523-1755.2000.00424.x.