Activation of STAT1 in Neurons Following Spinal Cord Injury in Mice

The signal transducer and activator of transcription 1 (STAT1) has been reported to be associated with neuronal cell death after cerebral ischemia. On the contrary, STAT3 has been revealed to regulate cell survival. We examined the chronological alteration and cellular localization of phosphorylated...

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Bibliographic Details
Published in:Neurochemical research 2011-12, Vol.36 (12), p.2236-2243
Main Authors: Osuka, Koji, Watanabe, Yasuo, Usuda, Nobuteru, Atsuzawa, Kimie, Yasuda, Muneyoshi, Aoshima, Chihiro, Wakabayashi, Toshihiko, Takayasu, Masakazu
Format: Article
Language:English
Subjects:
Animals
Biochemistry
Biomedical and Life Sciences
Biomedicine
Cell Biology
Enzyme Activation
Female
Janus Kinase 1 - metabolism
Mice
Neurochemistry
Neurology
Neurons - metabolism
Neurosciences
Original Paper
Phosphorylation
Signal Transduction - physiology
Spinal Cord Injuries - metabolism
STAT1 Transcription Factor - metabolism
STAT3 Transcription Factor - metabolism
Tyrosine - metabolism
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Summary:The signal transducer and activator of transcription 1 (STAT1) has been reported to be associated with neuronal cell death after cerebral ischemia. On the contrary, STAT3 has been revealed to regulate cell survival. We examined the chronological alteration and cellular localization of phosphorylated ( p )-JAK1, p -STAT1 and p -STAT3 following mild spinal cord injury (SCI) in mice. Western blot analysis indicated that JAK1 is significantly phosphorylated, accompanied by the phosphorylation of STAT1 at Tyr 701 within a similar timeframe. Immunofluorescence staining indicated that signal transduction of STAT3 is introduced into the nucleus of the neurons within the anterior horns; however, in mirror sections, that of STAT1 is limited to the cytoplasm. These findings suggest that STAT3 signal is predominantly transduced into the nucleus and plays a stronger role in neuronal survival than STAT1. Modulation of the functional balance between STAT1 and STAT3 might determine the survival or death of neurons after SCI.
ISSN:0364-3190
1573-6903
DOI:10.1007/s11064-011-0547-6