Remote Ischemic Postconditioning Promotes the Survival of Retinal Ganglion Cells after Optic Nerve Injury

Remote Ischemic Postconditioning Promotes the Survival of Retinal Ganglion Cells after Optic... Ischemic conditioning, the application of a mild ischemic stimulus to an ischemia-sensitive structure like the heart or brain either before (preconditioning) or after (postconditioning) its exposure to a lethal ischemic insult, is known to switch on endogenous protective mechanisms. However, most studies of its neuroprotective effect in the central nervous system (CNS) have focused on ischemic damage or related conditions like hypoxia, while its potential in treating other neural diseases remains uncertain. In particular, the recent discovery of remote ischemic postconditioning whereby mild ischemia applied to a region remote from the target after the main ischemic insult also confers protection offers an attractive paradigm to study its potential in other types of neural injury. Retinal ganglion cells damaged by optic nerve transection undergo extensive cell death. However, application of a series of mild ischemic/reperfusion cycles to the hind limb (limb remote ischemic postconditioning) at 10 min or 6 h after optic nerve cut was found to promote ganglion cell survival at 7 days post-injury, with the 10 min postconditioning still exerting protection at 14 days post-injury. Concomitant with the increased ganglion cell survival, 51 % more ganglion cells expressed the small heat shock protein HSP27, when remote ischemic postconditioning was performed at 10 min post-injury, as compared to the sham conditioning group. Our results highlight the potential of using remote ischemic postconditioning as a noninvasive neuroprotective strategy in different CNS disorders like spinal cord and traumatic brain injury. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Molecular Neuroscience Springer Journals

Remote Ischemic Postconditioning Promotes the Survival of Retinal Ganglion Cells after Optic Nerve Injury

Journal of Molecular Neuroscience, Volume 51 (3) – Jun 5, 2013

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Publisher
Springer Journals
Copyright
Copyright © 2013 by Springer Science+Business Media New York
Subject
Biomedicine; Neurosciences; Neurochemistry; Cell Biology; Proteomics; Neurology
ISSN
0895-8696
eISSN
1559-1166
DOI
10.1007/s12031-013-0036-2
pmid
23733254
Publisher site
See Article on Publisher Site

Abstract

Ischemic conditioning, the application of a mild ischemic stimulus to an ischemia-sensitive structure like the heart or brain either before (preconditioning) or after (postconditioning) its exposure to a lethal ischemic insult, is known to switch on endogenous protective mechanisms. However, most studies of its neuroprotective effect in the central nervous system (CNS) have focused on ischemic damage or related conditions like hypoxia, while its potential in treating other neural diseases remains uncertain. In particular, the recent discovery of remote ischemic postconditioning whereby mild ischemia applied to a region remote from the target after the main ischemic insult also confers protection offers an attractive paradigm to study its potential in other types of neural injury. Retinal ganglion cells damaged by optic nerve transection undergo extensive cell death. However, application of a series of mild ischemic/reperfusion cycles to the hind limb (limb remote ischemic postconditioning) at 10 min or 6 h after optic nerve cut was found to promote ganglion cell survival at 7 days post-injury, with the 10 min postconditioning still exerting protection at 14 days post-injury. Concomitant with the increased ganglion cell survival, 51 % more ganglion cells expressed the small heat shock protein HSP27, when remote ischemic postconditioning was performed at 10 min post-injury, as compared to the sham conditioning group. Our results highlight the potential of using remote ischemic postconditioning as a noninvasive neuroprotective strategy in different CNS disorders like spinal cord and traumatic brain injury.

Journal

Journal of Molecular NeuroscienceSpringer Journals

Published: Jun 5, 2013

References

  • Intraocular elevation of cyclic AMP potentiates ciliary neurotrophic factor-induced regeneration of adult rat retinal ganglion cell axons
    Cui, Q; Yip, HK; Zhao, RC; So, KF; Harvey, AR
  • CNS injury, glial scars, and inflammation: inhibitory extracellular matrices and regeneration failure
    Fitch, MT; Silver, J
  • Limb remote ischemic postconditioning protects against focal ischemia in rats
    Ren, C; Yan, Z; Wei, D; Gao, X; Chen, X; Zhao, H
  • Endogenous neuroprotection in the retina
    Roth, S
  • Neuronal intrinsic barriers for axon regeneration in the adult CNS
    Sun, F; He, Z

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