PMID- 16410269
OWN - NLM
STAT- MEDLINE
DCOM- 20060707
LR  - 20220408
IS  - 0931-0509 (Print)
IS  - 0931-0509 (Linking)
VI  - 21
IP  - 5
DP  - 2006 May
TI  - Macrophages contribute to the initiation of ischaemic acute renal failure in 
      rats.
PG  - 1231-9
AB  - BACKGROUND: Although neutrophils and T cells are important in mediating renal 
      injury following ischaemia/reperfusion, the role of macrophages is still unknown. 
      Using liposomal clodronate (LC), we investigated the effect of systemic 
      monocyte-macrophage depletion on renal damage in ischaemic acute renal failure in 
      rats. METHODS: Male Sprague-Dawley rats were injected by LC or liposomal vehicle 
      and underwent bilateral renal pedicle clamping (40 min) or sham ischaemia. 
      Biochemical and histological renal damage was assessed and gene expression 
      kinetics of tumour necrosis factor-alpha (TNF-alpha), interleukin-1beta 
      (IL-1beta), IL-6 and monocyte chemoattractant protein-1 (MCP-1) using 
      quantitative real-time reverse transcription-polymerase chain reaction were 
      conducted at 4, 24 and 72 h after reperfusion. RESULTS: The percentage of 
      peripheral blood monocytes and ectodysplasin-1-positive cells in liver decreased 
      significantly in LC-treated animals at 24 h. Systemic monocyte-macrophage 
      depletion resulted in (a) less severe tubular necrosis, (b) reduced inflammation 
      and (c) reduced apoptosis of renal tubular epithelial cells. Gene expression 
      kinetics showed that IL-6 gene expression peaked early at 4 h after reperfusion, 
      followed by TNF-alpha, IL-1beta and MCP-1 expressions, which peaked at 24 h. 
      Systemic monocyte-macrophage depletion significantly reduced these cytokine and 
      chemokine gene expressions. CONCLUSIONS: These results suggest that macrophages 
      are an important mediator in the initiation period of ischaemia/reperfusion 
      injury and strategies that limit initial macrophage infiltration or activation 
      can be useful in the treatment of acute renal failure.
FAU - Jo, Sang-Kyung
AU  - Jo SK
AD  - Division of Nephrology, Department of Internal Medicine, Korea University 
      Hospital, Anam-Dong, Sungbuk-Ku, Seoul 136-705, Korea.
FAU - Sung, Su-Ah
AU  - Sung SA
FAU - Cho, Won-Yong
AU  - Cho WY
FAU - Go, Kang-Jee
AU  - Go KJ
FAU - Kim, Hyoung-Kyu
AU  - Kim HK
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20060112
PL  - England
TA  - Nephrol Dial Transplant
JT  - Nephrology, dialysis, transplantation : official publication of the European 
      Dialysis and Transplant Association - European Renal Association
JID - 8706402
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Acute Kidney Injury/*pathology/physiopathology
MH  - Animals
MH  - *Apoptosis
MH  - Biopsy, Needle
MH  - Cell Proliferation
MH  - Disease Models, Animal
MH  - Immunohistochemistry
MH  - In Situ Nick-End Labeling
MH  - Interleukin-1/analysis/metabolism
MH  - Interleukin-6/analysis/metabolism
MH  - Kidney Function Tests
MH  - Macrophages/*cytology/physiology
MH  - Male
MH  - Probability
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reference Values
MH  - Reperfusion Injury/*pathology/physiopathology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Statistics, Nonparametric
MH  - Tumor Necrosis Factor-alpha/analysis/metabolism
EDAT- 2006/01/18 09:00
MHDA- 2006/07/11 09:00
CRDT- 2006/01/18 09:00
PHST- 2006/01/18 09:00 [pubmed]
PHST- 2006/07/11 09:00 [medline]
PHST- 2006/01/18 09:00 [entrez]
AID - gfk047 [pii]
AID - 10.1093/ndt/gfk047 [doi]
PST - ppublish
SO  - Nephrol Dial Transplant. 2006 May;21(5):1231-9. doi: 10.1093/ndt/gfk047. Epub 
      2006 Jan 12.