Peroxisomal biogenesis in ischemic brain

Jennifer M. Young, Jonathan W. Nelson, Jian Cheng, Wenri Zhang, Sarah Mader, Catherine Davis, Richard S. Morrison, Nabil Alkayed

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Aims: Peroxisomes are highly adaptable and dynamic organelles, adjusting their size, number, and enzyme composition to changing environmental and metabolic demands. We determined whether peroxisomes respond to ischemia, and whether peroxisomal biogenesis is an adaptive response to cerebral ischemia. Results: Focal cerebral ischemia induced peroxisomal biogenesis in peri-infarct neurons, which was associated with a corresponding increase in peroxisomal antioxidant enzyme catalase. Peroxisomal biogenesis was also observed in primary cultured cortical neurons subjected to ischemic insult induced by oxygen-glucose deprivation (OGD). A catalase inhibitor increased OGD-induced neuronal death. Moreover, preventing peroxisomal proliferation by knocking down dynamin-related protein 1 (Drp1) exacerbated neuronal death induced by OGD, whereas enhancing peroxisomal biogenesis pharmacologically using a peroxisome proliferator-activated receptor-alpha agonist protected against neuronal death induced by OGD. Innovation: This is the first documentation of ischemia-induced peroxisomal biogenesis in mammalian brain using a combined in vivo and in vitro approach, electron microscopy, high-resolution laser-scanning confocal microscopy, and super-resolution structured illumination microscopy. Conclusion: Our findings suggest that neurons respond to ischemic injury by increasing peroxisome biogenesis, which serves a protective function, likely mediated by enhanced antioxidant capacity of neurons. Antioxid. Redox Signal. 22, 109-120.

Original languageEnglish (US)
Pages (from-to)109-120
Number of pages12
JournalAntioxidants and Redox Signaling
Volume22
Issue number2
DOIs
StatePublished - Jan 10 2015

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Neurons
Peroxisomes
Brain
Oxygen
Glucose
Brain Ischemia
Catalase
Ischemia
Antioxidants
Dynamins
PPAR alpha
Confocal microscopy
High resolution electron microscopy
Enzymes
Lighting
Confocal Microscopy
Documentation
Organelles
Oxidation-Reduction
Microscopy

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology
  • Physiology
  • Clinical Biochemistry

Cite this

Peroxisomal biogenesis in ischemic brain. / Young, Jennifer M.; Nelson, Jonathan W.; Cheng, Jian; Zhang, Wenri; Mader, Sarah; Davis, Catherine; Morrison, Richard S.; Alkayed, Nabil.

In: Antioxidants and Redox Signaling, Vol. 22, No. 2, 10.01.2015, p. 109-120.

Research output: Contribution to journalArticle

Young, JM, Nelson, JW, Cheng, J, Zhang, W, Mader, S, Davis, C, Morrison, RS & Alkayed, N 2015, 'Peroxisomal biogenesis in ischemic brain', Antioxidants and Redox Signaling, vol. 22, no. 2, pp. 109-120. https://doi.org/10.1089/ars.2014.5833
Young JM, Nelson JW, Cheng J, Zhang W, Mader S, Davis C et al. Peroxisomal biogenesis in ischemic brain. Antioxidants and Redox Signaling. 2015 Jan 10;22(2):109-120. https://doi.org/10.1089/ars.2014.5833
Young, Jennifer M. ; Nelson, Jonathan W. ; Cheng, Jian ; Zhang, Wenri ; Mader, Sarah ; Davis, Catherine ; Morrison, Richard S. ; Alkayed, Nabil. / Peroxisomal biogenesis in ischemic brain. In: Antioxidants and Redox Signaling. 2015 ; Vol. 22, No. 2. pp. 109-120.
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