Mitochondrial dihydrolipoamide dehydrogenase is upregulated in response to intermittent hypoxic preconditioning

Rongrong Li, Xiaoting Luo, Jinzi Wu, Nopporn Thangthaeng, Marianna E. Jung, Siqun Jing, Linya Li, Dorette Z. Ellis, Li Liu, Zhengnian Ding, Michael J. Forster, Liang Jun Yan

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


Intermittent hypoxia preconditioning (IHP) has been shown to protect neurons against ischemic stroke injury. Studying how proteins respond to IHP may identify targets that can help fight stroke. The objective of the present study was to investigate whether mitochondrial dihydrolipoamide dehydrogenase (DLDH) would respond to IHP and if so, whether such a response could be linked to neuroprotection in ischemic stroke injury. To do this, we subjected male rats to IHP for 20 days and measured the content and activity of DLDH as well as the three α-keto acid dehydrogenase complexes that contain DLDH. We also measured mitochondrial electron transport chain enzyme activities. Results show that DLDH content was indeed upregulated by IHP and this upregulation did not alter the activities of the three α-keto acid dehydrogenase complexes. Results also show that the activities of the five mitochondrial complexes (I-V) were not altered either by IHP. To investigate whether IHP-induced DLDH upregulation is linked to neuroprotection against ischemic stroke injury, we subjected both DLDH deficient mouse and DLDH transgenic mouse to stroke surgery followed by measurement of brain infarction volume. Results indicate that while mouse deficient in DLDH had exacerbated brain injury after stroke, mouse overexpressing human DLDH also showed increased brain injury after stroke. Therefore, the physiological significance of IHP-induced DLDH upregulation remains to be further investigated.

Original languageEnglish
Pages (from-to)432-440
Number of pages9
JournalInternational Journal of Medical Sciences
Issue number5
StatePublished - 23 May 2015


  • Dihydrolipoamide dehydrogenase
  • Intermittent hypoxic preconditioning
  • Ischemic stroke
  • Mitochondria
  • Neuroprotection


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