Identification of genes differentially expressed in canine vasospastic cerebral arteries after subarachnoid hemorrhage

J Cereb Blood Flow Metab. 1999 Nov;19(11):1279-88. doi: 10.1097/00004647-199911000-00013.

Abstract

To understand the molecular processes of continuous vasospasm of cerebral arteries after subarachnoid hemorrhage, mRNA differential display and screening of cDNA expression array were performed to identify genes that are differentially expressed in vasospastic arteries of canine two-hemorrhage models. The expression levels of 18 genes were found to be upregulated, and those of two genes to be downregulated. Of these, 12 represent known genes or homologues of genes characterized previously, and the other eight genes are not related to any sequences in the databases. The known genes include five upregulated inflammation-related genes encoding monocyte chemotactic protein-1, cystatin B, inter-alpha-trypsin inhibitor family heavy chain-related protein, serum amyloid A protein, and glycoprotein 130, suggesting that inflammatory reaction may be involved in the development of cerebral vasospasm. The upregulation of three known genes encoding stress-related proteins of vascular endothelial growth factor, BiP protein, and growth-arrest and DNA-damage-inducible protein may be involved in possible cell survival in the damaged arteries. A full-length cDNA for the unknown clone DVS 27, whose expression was most highly upregulated, was isolated from the cerebral artery cDNA library by hybridization. Characterization of these genes should help to clarify the molecular mechanism of continuous cerebral vasospasm after subarachnoid hemorrhage.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Cerebral Arteries / metabolism*
  • Cerebral Arteries / physiopathology
  • DNA, Complementary / analysis
  • DNA, Complementary / genetics*
  • Dogs
  • Gene Expression*
  • Molecular Sequence Data
  • Subarachnoid Hemorrhage / genetics*
  • Subarachnoid Hemorrhage / metabolism
  • Subarachnoid Hemorrhage / physiopathology

Substances

  • DNA, Complementary