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- Title
Issue Cover (August 2015).
- Abstract
Front cover: Argon inhalation after retinal ischemia and reperfusion injury rescued retinal ganglien cells from death. Argons neuroprotective properties thereby comprise the induction of ERK‐1/2 phosphorylation. Immunohistochemistry with anti‐pERK‐1/2 (green fluorescence) and anti‐GFAP (red fluorescence) unveiled that pERK‐1/2 was upregulated in Müller cells (cell bodies in the inner nuclear layer and processes expanding the whole retina) 24 h after ischemia and reperfusion and Argon treatment. The mechanism, by which Argon exerts ist neuroprotective effects are ‐ at least in part ‐ mediated by the mitogen activated protein kinase ERK‐1/2. Inhibition of ERK‐1/2 results in a reduction of the anti‐apoptotic effects of Argon. Focussing the crucial neuron‐glia‐crosstalk, Argon may be considered as a treatment opportunity in ischemia induced neurodegeneration. Read the full article ‘Neuroprotective effects of Argon are mediated via an ERK‐1/2 dependent regulation of hemeoxygenase‐1 in retinal ganglion cells’ by F. Ulbrich, K. B. Kaufmann, M. Coburn, W. Alexander Lagrèze, M. Roesslein, J. Biermann, H. Buerkle, T. Loop and U. Goebel (J. Neurochem. 2015, vol. 134 (4), pp. 717–727) on doi: 10.1111/jnc.13115
- Subjects
JOURNAL of Neurochemistry (Periodical); MAGAZINE covers; RETINAL diseases
- Publication
Journal of Neurochemistry, 2015, Vol 134, Issue 4, pn/a
- ISSN
0022-3042
- Publication type
Article
- DOI
10.1111/jnc.12896