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Effects of repeated restraint stress on platelet endothelial cell adhesion molecule-1 immunoreactivity and protein levels in the gerbil hippocampus after transient cerebral ischemia
Stress has long been known to be a causative factor of various disease states. In this study, we investigated the effects of repeated restraint stress on platelet endothelial cell adhesion molecule-1 (PECAM-1), a very important mediator in inflammation, immunoreactivity and protein levels as well as...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Korean Association of Anatomists
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998780/ https://www.ncbi.nlm.nih.gov/pubmed/21190005 http://dx.doi.org/10.5115/acb.2010.43.1.54 |
Sumario: | Stress has long been known to be a causative factor of various disease states. In this study, we investigated the effects of repeated restraint stress on platelet endothelial cell adhesion molecule-1 (PECAM-1), a very important mediator in inflammation, immunoreactivity and protein levels as well as neuronal damage, in the gerbil hippocampus after 5 minutes of transient cerebral ischemia. Transient ischemia-induced neuronal death was shown in CA1 pyramidal cells 4 days after ischemia/reperfusion. However, repeated restraint stress protected neuronal death induced by ischemic damage. In the ischemia-group, PECAM-1 immunoreactivity and its protein levels were significantly increased in all the hippocampal subregions 4 days after ischemia/reperfusion. However, PECAM-1 immunoreactivity and its protein levels did not change significantly in the hippocampus of the stress-ischemia-group compared to the sham-groups. These results indicate that repeated restraint stress protects neuronal damage induced by transient cerebral ischemia, and this may be associated with maintenance of PECAM-1levels. |
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