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Open AccessJournal ArticleDOI

Hypoxic preconditioning induces changes in HIF-1 target genes in neonatal rat brain.

TLDR
Examination of the brains of newborn rats after exposure to hypoxia or CoCl2 afforded a 96% and 76% brain protection, respectively, compared with littermate control animals, suggesting that different molecular mechanisms may be involved in the induction of tolerance by Hypoxia and CoCl 2 in newborn brain.
Abstract
Hypoxic preconditioning induces tolerance to hypoxic-ischemic injury in neonatal rat brain and is associated with changes in gene expression Hypoxia-inducible factor-1 (HIF-1) is a transcription f

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Ischemic tolerance and endogenous neuroprotection

TL;DR: Although investigated for some time in model organisms, IP/IT has recently been shown in human brain and opens a window into endogenous neuroprotection and, potentially, a window of opportunity to utilize these mechanisms in the clinic to treat patients with stroke and other CNS disorders.
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Cerebral preconditioning and ischaemic tolerance

TL;DR: Current understanding of how 'preconditioning' stimuli trigger a cerebroprotective state known as cerebral 'ischaemic tolerance' is summarized.
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Physiological control of immune response and inflammatory tissue damage by hypoxia-inducible factors and adenosine A2A receptors.

TL;DR: A2A receptor-triggered generation of intracellular cAMP inhibits activated immune cells in a delayed negative feedback manner to prevent additional tissue damage, and targeting A2A adenosine receptors may have important clinical applications.
Journal ArticleDOI

HIF1 and oxygen sensing in the brain

TL;DR: Some of the molecular mechanisms of oxygen sensing in the brain are discussed, with particular emphasis on the oxygen-dependant regulation of the transcription factor HIF1 (hypoxia-inducible factor 1) — one of the main cellular responses to hypoxia that operates in numerous cell types.
Journal ArticleDOI

Normobaric hypoxia induces tolerance to focal permanent cerebral ischemia in association with an increased expression of hypoxia-inducible factor-1 and its target genes, erythropoietin and VEGF, in the adult mouse brain.

TL;DR: The authors' findings show that hypoxia elicits a delayed, short-lasting (<72 hours) tolerance to focal permanent ischemia in the adult mouse brain, and this model might be a useful paradigm to further study the mechanisms of ischemic tolerance, to identify new therapeutic targets for stroke.
References
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Journal ArticleDOI

Hypoxia-inducible factor 1 is a basic-helix-loop-helix-PAS heterodimer regulated by cellular O2 tension

TL;DR: Hypoxia-inducible factor 1 (HIF-1) is found in mammalian cells cultured under reduced O2 tension and is necessary for transcriptional activation mediated by the erythropoietin gene enhancer in hypoxic cells.
Journal ArticleDOI

Regulation of hypoxia-inducible factor 1α is mediated by an O2-dependent degradation domain via the ubiquitin-proteasome pathway

TL;DR: The identification of an oxygen-dependent degradation (ODD) domain within HIF-1alpha that controls its degradation by the ubiquitin-proteasome pathway is reported and may provide a means of controlling gene expression by changes in oxygen tension.
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The influence of immaturity on hypoxic-ischemic brain damage in the rat

TL;DR: Brain damage in the Levine preparation (unilateral common carotid artery ligation with hypoxia) consists of ischemic neuronal alterations in the ipsilateral forebrain in 7‐day‐postnatal rats.
Journal ArticleDOI

Purification and Characterization of Hypoxia-inducible Factor 1

TL;DR: The biochemical purification of HIF-1 from Epo-producing Hep3B cells and non-Epo-producing HeLa S3 cells concludes that in both cobalt chloride-treated HeLa cells and hypoxic Hep3 B cells HIF -1 is composed of two different subunits: 120-kDa Hif-1α and 91-94-k da HIF,1β.
Journal ArticleDOI

Transcriptional regulation of genes encoding glycolytic enzymes by hypoxia-inducible factor 1.

TL;DR: In this article, the role of HIF-1 as a mediator of adaptive responses to hypoxia that underlie cellular and systemic oxygen homeostasis was investigated in Hep3B cells.
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