Medical Journals

Epha4 Regulates Central Nervous System Vascular Formation.

Authors:
  • Goldshmit Yona
  • Galea Mary P
  • Bartlett Perry F
  • Turnley Ann M

From: Centre for Neuroscience, The University of Melbourne, Melbourne, Victoria 3010, Australia.

The Journal of comparative neurology

  • Publish Date: Aug 2006
  • ISSN: 0021-9967
  • Volume: 497
  • Issue: 6
  • Pages: 864-75
  • Medium: Print
  • Language: English
  • Citation (JAMA): Goldshmit Yona, Galea Mary P, Bartlett Perry F, et al. Epha4 Regulates Central Nervous System Vascular Formation.. J. Comp. Neurol. Aug 2006;497:864-75

Abstract

Molecules involved in axon guidance have recently also been shown to play a role in blood vessel guidance. To examine whether axon guidance molecules, such as the EphA4 receptor tyrosine kinase, might also play a role in development of the central nervous system (CNS) vasculature and repair following CNS injury, we examined wild-type and EphA4 null mutant (-/-) mice. EphA4-/- mice exhibited an abnormal CNS vascular structure in both the cerebral cortex and the spinal cord, with disorganized branching and a 30% smaller diameter. During development, EphA4 was expressed on endothelial cells. This pattern of expression was not maintained in the adult. After spinal cord injury in wild-type mice, expression of EphA4 was markedly up-regulated on activated astrocytes, many of which were tightly associated with blood vessels. In EphA4-/- spinal cord following injury, astrocytes were not as tightly associated with blood vessels as the wild-type astrocytes. In uninjured EphA4-/- mice, the blood-brain barrier (BBB) appeared normal, but it showed prolonged leakage following spinal cord injury. These results support a role for EphA4 in CNS vascular formation and guidance during development and an additional role in BBB repair.

Mesh Headings (Keywords): Animals, Blood-Brain Barrier, Brain, Central Nervous System, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Receptor, EphA4, Spinal Cord


Check for Full Text / PubMed Unique Identifier (PMID): 16802330


This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.

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The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.


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