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Related Concept Videos

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Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
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Hypoxia is a medical condition characterized by an inadequate oxygen supply to body tissues. It typically manifests as a bluish discoloration of the skin and mucosae, especially in fair-skinned individuals, when hemoglobin (Hb) saturation drops below 75%.
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Induction of Hypoxia in Living Frog and Zebrafish Embryos
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Activin A regulation under global hypoxia in developing mouse brain.

Florian A Brackmann1, Andrea S Link, Susan Jung

  • 1Department of Pediatrics, Friedrich-Alexander Universität Erlangen-Nürnberg, Loschgestrasse 15, 91054 Erlangen, Germany. florian.brackmann@uk-erlangen.de

Brain Research
|August 7, 2013
PubMed
Summary
This summary is machine-generated.

Activin A, a neuroprotective factor, is not upregulated in the brain during pure hypoxia. This suggests pure hypoxia does not activate this protective response, unlike other brain injuries.

Keywords:
ActivinHIFHypoxiaNeonatal brain injuryStrain difference

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Developmental Biology

Background:

  • Activin A is a growth factor with neuroprotective properties, upregulated in brain injuries like epilepsy, stroke, and trauma.
  • Activin A is a potential marker for perinatal hypoxic-ischemic brain injury severity.

Purpose of the Study:

  • To investigate activin A regulation under global hypoxia without ischemia.
  • To examine the effects of hypoxia on activin A expression in primary cortical neurons and in neonatal and adult mice.

Main Methods:

  • Primary cultures of cortical neurons and neonatal/adult mice (C57BL/6 and CD-1 strains) were used.
  • Moderate (11% O2, 2h) and severe (8% O2, 6h) hypoxia conditions were applied.
  • In situ hybridization, mRNA, and protein level analyses were performed. Hypoxia-inducible factors were pharmacologically stabilized.

Main Results:

  • Hypoxia did not increase, and sometimes decreased, activin βA (Inhba) mRNA and protein levels.
  • In situ hybridization showed no regional differences in Inhba expression related to hypoxia.
  • Pharmacologic stabilization of hypoxia-inducible factors did not alter Inhba mRNA levels.

Conclusions:

  • Pure hypoxia, unlike other brain injuries, does not appear to recruit activin A as an endogenous neuroprotective agent.
  • The expression of activin A is unresponsive to hypoxia in the developing and adult brain.