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Neuron, Available online 29 October 2015 | doi:10.1016/j.neuron.2015.09.050
Activating Injury-Responsive Genes with Hypoxia Enhances Axon Regeneration through Neuronal HIF-1α
Abstract
Yongcheol Cho,1,3 Jung Eun Shin,2 Eric Edward Ewan,1 Young Mi Oh,1 Wolfgang Pita-Thomas,1 and Valeria Cavalli1,*
1 Department of Anatomy and Neurobiology, School of Medicine, Washington University in St. Louis, St. Louis, MO 63110, USA
2 Department of Developmental Biology, School of Medicine, Washington University in St. Louis, St. Louis, MO 63110, USA
2 Department of Developmental Biology, School of Medicine, Washington University in St. Louis, St. Louis, MO 63110, USA
3Present address: School of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Republic of Korea
*Correspondence: Valeria Cavalli
Summary
Injured peripheral neurons successfully activate a proregenerative transcriptional program to enable axon regeneration and functional recovery. How transcriptional regulators coordinate the expression of such program remains unclear. Here we show that hypoxia-inducible factor 1α (HIF-1α) controls multiple injury-induced genes in sensory neurons and contribute to the preconditioning lesion effect. Knockdown of HIF-1α in vitro or conditional knock out in vivo impairs sensory axon regeneration. The HIF-1α target gene Vascular Endothelial Growth Factor A (VEGFA) is expressed in injured neurons and contributes to stimulate axon regeneration. Induction of HIF-1α using hypoxia enhances axon regeneration in vitro and in vivo in sensory neurons. Hypoxia also stimulates motor neuron regeneration and accelerates neuromuscular junction re-innervation. This study demonstrates that HIF-1α represents a critical transcriptional regulator in regenerating neurons and suggests hypoxia as a tool to stimulate axon regeneration.
논문정보
- Research article
- 2015년 10월 (BRIC 등록일 2015-11-04)
- 국외 연구진
- 생명과학 > 신경생물학
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