Deficiency for the chemokine monocyte chemoattractant protein-1 aggravates tubular damage after renal ischemia/reperfusion injury

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...

Full description

Saved in:
Bibliographic Details
Published in:PloS one 2015-04, Vol.10 (4), p.e0123203-e0123203
Main Authors: Stroo, Ingrid, Claessen, Nike, Teske, Gwendoline J D, Butter, Loes M, Florquin, Sandrine, Leemans, Jaklien C
Format: Article
Language:English
Subjects:
Accumulation
Analgesics
Animals
Apoptosis
Apoptosis - genetics
Butter
Chemokine CCL2 - deficiency
Chemokine CCL2 - genetics
Chemokine CCL2 - metabolism
Chemokines
Cytokines - genetics
Cytokines - metabolism
Disease Models, Animal
Gene Expression
Genes, Lethal
Growth factors
Inflammatory response
Injuries
Ischemia
Kidney Tubules - metabolism
Kidney Tubules - pathology
Kidneys
Leukocytes - metabolism
Macrophages
Macrophages - metabolism
Male
Mice
Mice, Knockout
Migration
Neutrophils
Oxidative stress
Pathology
Peroxidase - metabolism
Proteins
Reperfusion Injury - genetics
Reperfusion Injury - metabolism
Reperfusion Injury - pathology
RNA, Messenger - genetics
RNA, Messenger - metabolism
Rodents
Stem cells
Surgery
Time Factors
Up-Regulation
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0123203