Expression of monocyte chemoattractant protein-1 and macrophage inflammatory protein-1 after focal cerebral ischemia in the rat

  title={Expression of monocyte chemoattractant protein-1 and macrophage inflammatory protein-1 after focal cerebral ischemia in the rat},
  author={Jong S. Kim and Subhash C. Gautam and Michael Chopp and Cecylia Zaloga and Michael L. Jones and Peter A. Ward and Kenneth M. A. Welch},
  journal={Journal of Neuroimmunology},
Overexpression of Monocyte Chemoattractant Protein 1 in the Brain Exacerbates Ischemic Brain Injury and is Associated with Recruitment of Inflammatory Cells
  • Yong Chen, J. Hallenbeck, S. Vogel
  • Biology, Medicine
    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 2003
Brain infarction volumes after ischemia were significantly larger in MBP-JE mice than in wild-type controls and were accompanied by increased local transmigration and perivascular accumulation of macrophages and neutrophils, indicating that MCP-1 can contribute to inflammatory injury in stroke.
Hypoxic-Ischemic Injury Induces Monocyte Chemoattractant Protein-1 Expression in Neonatal Rat Brain
The results suggest that in the developing brain, MCP-1 could represent a functionally important molecular signal for the microglial response to hypoxic-ischemic injury.
Chemokine and Inflammatory Cell Response to Hypoxia-Ischemia in Immature Rats
The expression of mRNA for α- and β-chemokines preceded the appearance of immune cells suggesting that these molecules may have a role in the inflammatory response to insults in the immature central nervous system.
Differential production of MCP‐1 and cytokine‐induced neutrophil chemoattractant in the ischemic brain after transient focal ischemia in rats
It is suggested that MCP‐1 in cerebral ischemia actually plays a significant role in the migration of macrophages into the lesion and that the differential temporal production of these chemokines contributes to the regulation of infiltrated leukocyte subtypes.
MIP-1alpha and MCP-1 Induce Migration of Human Umbilical Cord Blood Cells in Models of Stroke.
MCP-1 and MIP-1alpha expression were significantly increased in the ischemic hemisphere of brain, and significantly promoted HUCB cell migration compared to the contralateral side, suggesting that the increased chemokines in theIschemic area can bind cell surface receptors on H UCB, and induce cell infiltration of systemically delivered HUCBs cells into the CNS in vivo.


Monocyte chemoattractant protein-1 regulates adhesion molecule expression and cytokine production in human monocytes.
Results indicate that MCP-1 is not only a chemoattractant but also a novel cytokine with the capacity to regulate several parameters of monocyte function.
Interleukin-1 beta mRNA expression in ischemic rat cortex.
Brain interleukin-1 beta mRNA is elevated acutely after permanent focal ischemia and especially in hypertensive rats, suggesting that this potent proinflammatory and procoagulant cytokine might have a role in brain damage following ischemIA.
Cytokine-activated human endothelial cells synthesize and secrete a monocyte chemoattractant, MCP-1/JE.
The results suggest that endothelial cells secrete a monocyte chemoattractant, MCP-1/JE, in response to inflammatory mediators, and thus may contribute to the accumulation of monocytes at sites of inflammation.
Potential role of monocyte chemoattractant protein 1/JE in monocyte/macrophage-dependent IgA immune complex alveolitis in the rat.
We have examined the role of monocyte chemoattractant protein 1 (MCP 1) in the pathogenesis of monocyte/macrophage-dependent IgA immune complex alveolitis in the rat. Rat MCP 1 was cloned and
Human monocyte chemoattractant protein-1 (MCP-1).
Expression of cytokine-like genes JE and KC is increased during renal ischemia.
The expression of JE and KC, other growth-factor-responsive genes that code for small secreted glycoproteins with cytokine-like properties, which may play a role in inflammation are reported on.
The role of cytokines in the generation of inflammation and tissue damage in experimental gram-positive meningitis
These cytokines have multiple inflammatory activities in the central nervous system and contribute to tissue damage during pneumococcal meningitis, as suggested by a rabbit model of meningeal inflammation.
Macrophage inflammatory protein 1 modulates macrophage function.
Data reveal that MIP 1 peptides act as autocrine modulators of their cells of origin, and raise the possibility that Mip 1 peptide may play a role in modulating macrophage responses to inflammatory stimuli in vivo.
Interleukin-4 induces the synthesis and secretion of MCP-1/JE by human endothelial cells.
Results suggest that EC-produced MCP-1/JE may mediate some of IL-4's effects on monocyte physiology in vivo, including IL- 4's anti-tumor properties.