Monocyte chemoattractant protein-1 expression correlates with monocyte infiltration in the post-ischemic kidney

James C. Rice, Jeff S. Spence, Deborah L. Yetman, Robert L. Safirstein

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

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. 1 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.

Original languageEnglish (US)
Pages (from-to)703-723
Number of pages21
JournalRenal Failure
Volume24
Issue number6
DOIs
StatePublished - 2002

Fingerprint

Chemokine CCL2
Monocytes
Ischemia
Kidney
Peptides
Reperfusion
Reperfusion Injury
Messenger RNA
Urine Specimen Collection
Chemotactic Factors
Kidney Diseases
Chemokines
Acute Kidney Injury
Sprague Dawley Rats
Biomarkers
Macrophages
Urine

Keywords

  • Biomarker
  • Chemokine
  • Ischemia-reperfusion
  • Thick ascending limb

ASJC Scopus subject areas

  • Nephrology

Cite this

Monocyte chemoattractant protein-1 expression correlates with monocyte infiltration in the post-ischemic kidney. / Rice, James C.; Spence, Jeff S.; Yetman, Deborah L.; Safirstein, Robert L.

In: Renal Failure, Vol. 24, No. 6, 2002, p. 703-723.

Research output: Contribution to journalArticle

Rice, James C. ; Spence, Jeff S. ; Yetman, Deborah L. ; Safirstein, Robert L. / Monocyte chemoattractant protein-1 expression correlates with monocyte infiltration in the post-ischemic kidney. In: Renal Failure. 2002 ; Vol. 24, No. 6. pp. 703-723.
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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. 1 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.

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