Increased jun immunoreactivity in an in vitro model of mammalian spinal neuron physical injury.
Dendrites were transected from murine spinal neurons. Unlesioned neurons showed dark nucleolar and patchy cytoplasmic jun immunostaining. By 0.5 and 2 h, most lesioned neurons stained intensely throughout the soma. However, at 24 h only dead neurons displayed intense somal staining, and 100% of the surviving cells stained like unlesioned controls. Correlation of immunostaining patterns with viability, injury, and death suggests jun gene expression may influence the survival of neurons after physical injury.
Department of Neurosurgery, University of Pennsylvania, Philadelphia, USA.
R
R
Raghupathi
I
I
Grants
L J
LJ
Rosenberg
T K
TK
McIntosh
J H
JH
Lucas
D000818:Animals; D015415:Biomarkers; D016923:Cell Death / Q000502:physiology; D002470:Cell Survival; D002478:Cells, Cultured; D004195:Disease Models, Animal; D015870:Gene Expression; D017781:Genes, Immediate-Early / Q000502:physiology*; D016758:Genes, jun / Q000502:physiology*; D051379:Mice; D008858:Microscopy, Phase-Contrast; D009410:Nerve Degeneration / Q000378:metabolism* / Q000473:pathology; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D016755:Proto-Oncogene Proteins c-jun / Q000096:biosynthesis*; D013116:Spinal Cord / Q000196:embryology / Q000378:metabolism* / Q000473:pathology; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000473:pathology; D013997:Time Factors
D015415:Biomarkers; D016755:Proto-Oncogene Proteins c-jun