作者: Wulf Paschen , Ido Yatsiv , Shai Shoham , Esther Shohami
DOI: 10.1046/J.1471-4159.2003.02218.X
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摘要: Brain trauma was induced in mice using a closed head injury (CHI) model. At 1, 6 or 24 h after trauma, brains were dissected into the cortex, striatum and hippocampus. Changes levels of processed X-box protein 1 (xbp1), glucose-regulated 78 (grp78), growth arrest DNA damage-inducible gene 153 (gadd153) heat-shock 70 (hsp70) mRNA, indicating impaired endoplasmic reticulum (ER) cytoplasmic functioning, evaluated by quantitative PCR. In xbp1 mRNA rose to 2000% control CHI, stayed high throughout experiments. hippocampus striatum, delayed fashion, peaking at (1000% control) CHI (1500% respectively. Levels grp78 only slightly increased cortex (150% control), unchanged transiently decreased striatum. gadd153 did not change significantly trauma. A transient rise hsp70 observed (600% control). Processing is sign activation unfolded response indicative ER dysfunction. The results suggest that brain induces dysfunction, which spreads from ipsilateral These observations may have clinical implications should therefore be considered for future investigations on therapeutic intervention caused contusion-induced neurotrauma.