PMID- 25875776
OWN - NLM
STAT- MEDLINE
DCOM- 20160118
LR  - 20190223
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 10
IP  - 4
DP  - 2015
TI  - Deficiency for the chemokine monocyte chemoattractant protein-1 aggravates 
      tubular damage after renal ischemia/reperfusion injury.
PG  - e0123203
LID - 10.1371/journal.pone.0123203 [doi]
LID - e0123203
AB  - Temporal expression of chemokines is a crucial factor in the regulation of renal 
      ischemia/reperfusion (I/R) injury and repair. Beside their role in the migration 
      and activation of inflammatory cells to sites of injury, chemokines are also 
      involved in other processes such as angiogenesis, development and migration of 
      stem cells. In the present study we investigated the role of the chemokine MCP-1 
      (monocyte chemoattractant protein-1 or CCL2), the main chemoattractant for 
      monocytes, during renal I/R injury. MCP-1 expression peaks several days after 
      inducing renal I/R injury coinciding with macrophage accumulation. However, MCP-1 
      deficient mice had a significant decreased survival and increased renal damage 
      within the first two days, i.e. the acute inflammatory response, after renal I/R 
      injury with no evidence of altered macrophage accumulation. Kidneys and primary 
      tubular epithelial cells from MCP-1 deficient mice showed increased apoptosis 
      after ischemia. Taken together, MCP-1 protects the kidney during the acute 
      inflammatory response following renal I/R injury.
FAU - Stroo, Ingrid
AU  - Stroo I
AD  - Department of Pathology, Academic Medical Center, University of Amsterdam, 
      Amsterdam, The Netherlands.
FAU - Claessen, Nike
AU  - Claessen N
AD  - Department of Pathology, Academic Medical Center, University of Amsterdam, 
      Amsterdam, The Netherlands.
FAU - Teske, Gwendoline J D
AU  - Teske GJ
AD  - Department of Pathology, Academic Medical Center, University of Amsterdam, 
      Amsterdam, The Netherlands.
FAU - Butter, Loes M
AU  - Butter LM
AD  - Department of Pathology, Academic Medical Center, University of Amsterdam, 
      Amsterdam, The Netherlands.
FAU - Florquin, Sandrine
AU  - Florquin S
AD  - Department of Pathology, Academic Medical Center, University of Amsterdam, 
      Amsterdam, The Netherlands.
FAU - Leemans, Jaklien C
AU  - Leemans JC
AD  - Department of Pathology, Academic Medical Center, University of Amsterdam, 
      Amsterdam, The Netherlands.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150413
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (RNA, Messenger)
RN  - EC 1.11.1.7 (Peroxidase)
SB  - IM
MH  - Animals
MH  - Apoptosis/genetics
MH  - Chemokine CCL2/deficiency/*genetics/metabolism
MH  - Cytokines/genetics/metabolism
MH  - Disease Models, Animal
MH  - Gene Expression
MH  - Genes, Lethal
MH  - Kidney Tubules/*metabolism/pathology
MH  - Leukocytes/metabolism
MH  - Macrophages/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Knockout
MH  - Peroxidase/metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - Reperfusion Injury/*genetics/metabolism/pathology
MH  - Time Factors
MH  - Up-Regulation
PMC - PMC4395234
COIS- Competing Interests: The authors have delcared that no competing interests exist.
EDAT- 2015/04/16 06:00
MHDA- 2016/01/19 06:00
PMCR- 2015/04/13
CRDT- 2015/04/16 06:00
PHST- 2014/07/30 00:00 [received]
PHST- 2015/03/01 00:00 [accepted]
PHST- 2015/04/16 06:00 [entrez]
PHST- 2015/04/16 06:00 [pubmed]
PHST- 2016/01/19 06:00 [medline]
PHST- 2015/04/13 00:00 [pmc-release]
AID - PONE-D-14-31714 [pii]
AID - 10.1371/journal.pone.0123203 [doi]
PST - epublish
SO  - PLoS One. 2015 Apr 13;10(4):e0123203. doi: 10.1371/journal.pone.0123203. 
      eCollection 2015.