RESEARCH ARTICLE 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 inflam-matory cells to sites of injury, chemokines are also involved in other processes such as an-giogenesis, 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 with-in the first two days, i.e. the acute inflammatory response, after renal I/R injury with no evi-dence 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