Systemic hypoxia differentially affects neurogenesis during early mouse brain maturation

Brain Dev. 2012 Apr;34(4):261-73. doi: 10.1016/j.braindev.2011.07.006. Epub 2011 Aug 6.

Abstract

Background: Cerebral tissue oxygen level modifies crucial processes of neurogenesis, glial and neuronal development during physiological and hypoxic conditions. Whether hypoxia-sensitive factors such as doublecortin (DCX) and hypoxia-inducible transcription factor (HIF)-regulated CXCR4 and SDF-1 modify and activate adaptation to hypoxia in developing brain is not well understood. Present study investigated maturational regulation of oxygen-sensitive developmental genes and proteins in developing mouse brain in relation to the degree of hypoxia.

Methods: Physiological expression of HIF-1, CXCR4, SDF-1 and DCX were analyzed in the brain of C57/BL6 mice (P0-P60). In addition, mice (P0, P7) were exposed to normoxia, acute (8% O(2), 6 h) or chronic hypoxia (10% O(2), 7 d) followed by reoxygenation. Gene expression was analyzed by quantitative PCR, proteins were quantified by Western blot analysis and immunohistochemistry.

Results: Cerebral HIF-1α protein, CXCR4 and DCX mRNA levels showed maturational stage-related peak levels at P0/P1, whereas SDF-1 mRNA levels were highest at P17. CXCR4 and SDF-1 mRNA levels were not altered in response to hypoxia. Whereas DCX mRNA levels significantly increased during acute hypoxia, down-regulation of DCX transcripts was found in response to chronic hypoxia compared to controls, and these changes were related to specifically vulnerable brain regions.

Conclusions: Maturational stage-related dynamic changes of HIF-1α, CXCR4, SDF-1 and DCX may reflect involvement of hypoxia-regulated systems in important developmental regulatory processes of the developing brain. Extending the knowledge of differential effects of hypoxia on neurogenesis and dynamic regulatory networks present data provide a basis for future research on gestational age-specific neuroprotective options.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Animals
  • Animals, Newborn
  • Cell Differentiation / physiology*
  • Chemokine CXCL12 / biosynthesis
  • Chemokine CXCL12 / genetics
  • Chronic Disease
  • Disease Models, Animal
  • Doublecortin Domain Proteins
  • Doublecortin Protein
  • Female
  • Fetal Hypoxia / metabolism
  • Fetal Hypoxia / pathology*
  • Fetal Hypoxia / physiopathology*
  • Gene Expression Regulation, Developmental / physiology*
  • Hypoxia, Brain / metabolism
  • Hypoxia, Brain / pathology*
  • Hypoxia, Brain / physiopathology*
  • Hypoxia-Inducible Factor 1, alpha Subunit / physiology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Microtubule-Associated Proteins / biosynthesis
  • Microtubule-Associated Proteins / genetics
  • Neurogenesis / physiology*
  • Neuropeptides / biosynthesis
  • Neuropeptides / genetics
  • RNA, Messenger / biosynthesis
  • Receptors, CXCR4 / biosynthesis
  • Receptors, CXCR4 / genetics

Substances

  • CXCR4 protein, mouse
  • Chemokine CXCL12
  • Cxcl12 protein, mouse
  • Dcx protein, mouse
  • Doublecortin Domain Proteins
  • Doublecortin Protein
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Microtubule-Associated Proteins
  • Neuropeptides
  • RNA, Messenger
  • Receptors, CXCR4