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A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage
Published on: January 17, 2013
MMP-9 expression and activity is concurrent with endothelial cell apoptosis in the basilar artery after subarachnoid
Zongduo Guo1, Liang Xu, Xiaoying Wang
1Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China, stonegzd@gmail.com.
Abstract:
Subarachnoid hemorrhage refers to one kind of lethal stroke. While several studies have shown the role of matrix metalloproteinase 9 in cerebral tissues and microvasculature after subarachnoid hemorrhage the role of matrix metalloproteinase 9 in large cerebral vasculature is limited, The present study aimed at investigating the relationship between the expression and activity of matrix metalloproteinase 9 and vascular endothelial cell apoptosis in the basilar artery at early-stage post-subarachnoid hemorrhaging in rats. The expression and activity of matrix metalloproteinase 9 in the basilar artery increased at 12 h after subarachnoid hemorrhage and peaked at 24 h. Concurrently, the number of apoptotic cells in the basilar artery increased at 12 h and peaked at 24 h following subarachnoid hemorrhage. Additionally, laminin and cleaved caspase 3 reached to their lowest and highest levels at 24 h after subarachnoid hemorrhage, respectively. Our results suggested that the change in expression and activity of matrix metalloproteinase 9 paralleled that of apoptotic cells in the basilar artery following subarachnoid hemorrhage. Matrix metalloproteinase 9 may be contributing to the injury of the basilar artery after subarachnoid hemorrhage via laminin degradation. Although the underlying mechanisms need to be explored further, our study has shown a potential association of matrix metalloproteinase 9 with injury of the basilar artery and can be associated with early-stage brain injury following subarachnoid hemorrhage.
Insights
Matrix metalloproteinase 9 (MMP-9) activity increased in rat basilar arteries after subarachnoid hemorrhage, correlating with endothelial cell apoptosis. MMP-9 may contribute to early-stage basilar artery injury following this stroke type.
Area of Science:
- Neuroscience
- Vascular Biology
- Stroke Research
Background:
- Subarachnoid hemorrhage (SAH) is a severe stroke type.
- Matrix metalloproteinase 9 (MMP-9) is implicated in cerebral tissue and microvasculature injury post-SAH.
- The role of MMP-9 in large cerebral arteries after SAH remains less understood.
Purpose of the Study:
- To investigate the relationship between MMP-9 expression/activity and vascular endothelial cell apoptosis in the basilar artery.
- To examine early-stage changes following experimental SAH in rats.
Main Methods:
- Rats underwent induced subarachnoid hemorrhage.
- MMP-9 expression and activity were measured in the basilar artery.
- Vascular endothelial cell apoptosis was assessed.
- Levels of laminin and cleaved caspase-3 were quantified.
Main Results:
- MMP-9 expression and activity in the basilar artery increased at 12 hours and peaked at 24 hours post-SAH.
- Vascular endothelial cell apoptosis also increased at 12 hours and peaked at 24 hours.
- Laminin levels decreased while cleaved caspase-3 levels increased at 24 hours post-SAH.
Conclusions:
- MMP-9 expression and activity changes parallel endothelial cell apoptosis in the basilar artery after SAH.
- MMP-9 may contribute to basilar artery injury through laminin degradation.
- MMP-9 is potentially associated with early-stage brain injury following subarachnoid hemorrhage.
