Copyright © 2002 Rainald Schmidt-Kastner et al.

Abstract

Recently, a specific defense system against hypoxia has been described which uses the hypoxia-inducible factor-1 (HIF-1) as transcription factor. HIF-1 coordinates the response to prolonged hypoxia which pertains to glycolysis (e.g., lactate dehydrogenase = LDH-5), glucose transport, vasodilation, and angiogenesis[1]. The level of the HIF-1a subunit is oxygen-dependent, and the protein concentration is mainly regulated via degradation in the proteasome[1], involving a novel class of oxygen-sensing proline-4-hydroxylases[2]. HIF-1a combines with the constitutively expressed HIF-1ك protein to form HIF-1[1]. Ischemia and hypoxia of the brain are major events in cardiac arrest and stroke. In this report, we examined changes of HIF-1a mRNA and the target gene, LDH-5, in the forebrain of rats after transient global brain ischemia[3] or in chronic oligemia[4].