Peer-reviewed veterinary case report
MMP-9 expression and activity is concurrent with endothelial cell apoptosis in the basilar artery after subarachnoid hemorrhaging in rats.
- Journal:
- Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
- Year:
- 2015
- Authors:
- Guo, Zongduo et al.
- Affiliation:
- Department of Neurosurgery · China
- Species:
- rodent
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.
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Search related cases →Original publication: https://pubmed.ncbi.nlm.nih.gov/25627354/