Immunohistochemical analysis of TIMP-2 and collagen types I and IV in experimental spinal cord ischemia-reperfusion injury in rats.


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ANIK İ., Kokturk S., Genc H., Cabuk B., Koc K., YAVUZ Ş., ...More

The journal of spinal cord medicine, vol.34, no.3, pp.257-64, 2011 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 34 Issue: 3
  • Publication Date: 2011
  • Doi Number: 10.1179/107902611x12972448729648
  • Journal Name: The journal of spinal cord medicine
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.257-64
  • Keywords: Spinal cord ischemia, Collagen IV, TIMP-2, Paraplegia, Glial scar formation, BLOOD-BRAIN-BARRIER, FREE-RADICAL SCAVENGER, CENTRAL-NERVOUS-SYSTEM, MATRIX METALLOPROTEINASES, BASEMENT-MEMBRANE, CEREBRAL-ISCHEMIA, TISSUE INHIBITORS, EXTRACELLULAR-MATRIX, GENE-EXPRESSION, POTENTIAL ROLE
  • Kocaeli University Affiliated: Yes

Abstract

Background: Thoracic and thoracoabdominal aortic intervention carries a significant risk of spinal cord ischemia. The pathophysiologic mechanisms that cause hypoxic/ischemic injury to the spinal cord have not been totally explained. In normal spinal cord, neurons and glial cells do not express type IV collagen. Type IV collagen produced by reactive astrocytes is reported to participate in glial scar formation. Tissue inhibitors of metalloproteinases (TIMPs) are endogenous inhibitors that regulate the activity of the matrix metalloproteinases (MMPs). TIMP-2 binds strongly with MMP-2, facilitating activation by membrane-type MMP. Imbalance between TIMPs and MMPs can lead to excessive degradation of matrix components. Type IV collagen involved in the blood-brain barrier disruption and glial scar formation, TIMP-2 influences MMP-2 that controls degradation of collagen I and IV.