Hypoxia alters the expression of inhibitor of apoptosis proteins after brain trauma in the mouse
Autor: | Phillip Griffin, Nathalie H. Gendron, Rachel E. Shaye, Isabelle Gaboury, Sarah Kawesa, Zul Merali, Alex MacKenzie, Angelo Mikrogianakis, Julia Lockwood, James S. Hutchison |
---|---|
Rok vydání: | 2007 |
Předmět: |
Male
Programmed cell death medicine.medical_specialty Time Factors Apoptosis Inhibitor Traumatic brain injury Apoptosis Motor Activity Inhibitor of apoptosis Inhibitor of Apoptosis Proteins Mice Internal medicine medicine In Situ Nick-End Labeling Animals RNA Messenger Hypoxia Caspase biology Feeding Behavior Hypoxia (medical) medicine.disease nervous system diseases Mice Inbred C57BL Disease Models Animal Endocrinology nervous system Brain Injuries Immunology biology.protein Neurology (clinical) NAIP medicine.symptom |
Zdroj: | Journal of neurotrauma. 24(2) |
ISSN: | 0897-7151 |
Popis: | Hypoxia worsens brain injury following trauma, but the mechanisms remain unclear. The purpose of this study was to determine the effect of traumatic brain injury (TBI) and secondary hypoxia (9% oxygen) on apoptosis-related protein expression, cell death, and behavior. Using a murine weight-drop model, TBI led to an early (6 h) increase followed by a later (24 h) decrease in neuronal apoptosis inhibitor protein (NAIP) expression in the olfactory and motor cortex; in contrast, TBI led to a sustained (6 h to 7 days) increase in NAIP in the striatum. The peak increase in the expression of NAIP (6-12 h) following TBI alone was delayed (1-7 days) when hypoxia was added to TBI. Hypoxia following TBI further depleted other apoptosis inhibitor proteins (IAPs) and activated caspases, as well as increased contusion size and worsened cell death. Hypoxia added to TBI also increased motor and feeding activity on days 2 and 4 compared to TBI alone. Hypoxia without TBI had no effect on the expression of IAPs or cell death. These findings show that IAPs have a potential role in the increased vulnerability of brain cells to hypoxia following TBI, and have implications for configuring future therapies for TBI. |
Databáze: | OpenAIRE |
Externí odkaz: |
načítá se...