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Prothymosin α as robustness molecule against ischemic stress to brain and retina
Author(s) -
Ueda Hiroshi,
Matsunaga Hayato,
Uchida Hitoshi,
Ueda Mutsumi
Publication year - 2010
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2010.05466.x
Subject(s) - necrosis , apoptosis , programmed cell death , tumor necrosis factor alpha , ischemia , neuroscience , retina , biology , microbiology and biotechnology , medicine , pathology , immunology , biochemistry
Following stroke or traumatic damage, neuronal death via both necrosis and apoptosis causes loss of functions, including memory, sensory perception, and motor skills. As necrosis has the nature to expand, while apoptosis stops the cell death cascade in the brain, necrosis is considered to be a promising target for rapid treatment for stroke. We identified the nuclear protein, prothymosin alpha (ProTα) from the conditioned medium of serum‐free culture of cortical neurons as a key protein‐inhibiting necrosis. In the culture of cortical neurons in the serum‐free condition without any supplements, ProTα inhibited the necrosis, but caused apoptosis. In the ischemic brain or retina, ProTα showed a potent inhibition of both necrosis and apoptosis. By use of anti‐brain‐derived neurotrophic factor or anti‐erythropoietin IgG, we found that ProTα inhibits necrosis, but causes apoptosis, which is in turn inhibited by ProTα‐induced neurotrophins under the condition of ischemia. From the experiment using anti‐ProTα IgG or antisense oligonucleotide for ProTα, it was revealed that ProTα has a pathophysiological role in protecting neurons in stroke.