PMID- 12472194
OWN - NLM
STAT- MEDLINE
DCOM- 20030325
LR  - 20190516
IS  - 0886-022X (Print)
IS  - 0886-022X (Linking)
VI  - 24
IP  - 6
DP  - 2002 Nov
TI  - Monocyte chemoattractant protein-1 expression correlates with monocyte 
      infiltration in the post-ischemic kidney.
PG  - 703-23
AB  - Chemokines play a prominent role in the acute inflammatory response in several 
      models of kidney disease. We reported that monocyte chemotactic peptide-1 (MCP-1) 
      mRNA is increased by ischemia-reperfusion injury. In this report, we examined the 
      effects of ischemia-reperfusion injury on the kinetics and location of MCP-1 
      protein expression, the excretion of MCP- 1 protein in the urine and on the 
      infiltration of mononuclear cells in the kidney. Pair-fed Sprague-Dawley rats 
      underwent bilateral renal ischemia (50 min) or sham ischemia and placed in 
      metabolic cages for daily urine collections. Kidneys were harvested at d. 1, 3, 
      7, and 10 after ischemia-reperfusion (I-R) or sham-ischemia (S-I). Kidney MCP-1 
      mRNA levels were increased on d. I and 3 post-ischemia. Kidney MCP-1 protein 
      levels were increased in the I-R group on d. 1 and 3. MCP-1 expression occurred 
      predominantly in the distal tubule segments by immunohistology. There was an 
      increase in monocytes/macrophages infiltration in the I-R group, compared to the 
      S-I or controls by d. 1. Urinary MCP-1 excretion increased 3-fold in the I-R 
      group, and remained elevated above the S-I group and baseline levels, on d. 3 
      through d. 8. Kidney MCP-1 mRNA levels, protein levels and urinary MCP-1 
      excretion rates are increased by ischemia-reperfusion injury. The areas of 
      increase in MCP-1 chemoattractant expression correlates with an increase in 
      monocyte infiltration in the kidney. Although its pathophysiologic role remains 
      to be determined, MCP-1 may participate in, and be a biomarker for, the 
      mononuclear inflammatory processes that occur after ischemia-induced acute renal 
      failure.
FAU - Rice, James C
AU  - Rice JC
AD  - Department of Internal Medicine, The University of Texas Medical Branch at 
      Galveston, Galveston, TX 77555-0562, USA. jrice@utmb.edu
FAU - Spence, Jeff S
AU  - Spence JS
FAU - Yetman, Deborah L
AU  - Yetman DL
FAU - Safirstein, Robert L
AU  - Safirstein RL
LA  - eng
GR  - DK-54471-01/DK/NIDDK NIH HHS/United States
GR  - DK-58324/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Ren Fail
JT  - Renal failure
JID - 8701128
RN  - 0 (Biomarkers)
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Acute Kidney Injury/*genetics/*immunology/urine
MH  - Animals
MH  - Biomarkers/urine
MH  - Chemokine CCL2/*genetics/pharmacokinetics/*urine
MH  - Disease Models, Animal
MH  - Gene Expression/*genetics/*immunology
MH  - Male
MH  - Neutrophil Infiltration/*genetics/*immunology
MH  - RNA, Messenger/*analysis/*genetics/immunology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reperfusion Injury/*genetics/*immunology/urine
MH  - Severity of Illness Index
MH  - Time Factors
EDAT- 2002/12/11 04:00
MHDA- 2003/03/26 05:00
CRDT- 2002/12/11 04:00
PHST- 2002/12/11 04:00 [pubmed]
PHST- 2003/03/26 05:00 [medline]
PHST- 2002/12/11 04:00 [entrez]
AID - 10.1081/jdi-120015673 [doi]
PST - ppublish
SO  - Ren Fail. 2002 Nov;24(6):703-23. doi: 10.1081/jdi-120015673.