Abstract
Early brain injury is now considered as an important cause of delayed neurological deterioration after aneurysmal subarachnoid hemorrhage (SAH), and neuronal apoptosis is one of the constituents of early brain injury. Caspase family is popular proteases in apoptotic pathways, but there also exist caspase-independent cell death pathways in many pathologic states. In this study, we investigated the ratio of caspase-related and caspase-unrelated neuronal deaths in a mice endovascular perforation SAH model. At 24 h after SAH, about half of neurons in the perforation-side cortex showed increased cleaved caspase-3 immunoreactivity. On the other hand, about half of cleaved caspase-3-immunonegative neurons showed abnormal morphology, suggesting that they were in the process of some sort of cell death in the absence of caspase-3 activity. These findings suggest that both caspase-dependent and caspase-independent signaling pathways may cause neuronal death after SAH.
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Acknowledgment
This work was supported in part by a grant-in-aid for Scientific Research from Japan Society for the Promotion of Science to Drs. Shiba and Suzuki. We thank Chiduru Yamamoto (Department of Neurosurgery, Mie University Graduate School of Medicine) for her assistance.
Conflicts of Interest: We declare that we have no conflict of interest.
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Nakano, F. et al. (2020). Possible Involvement of Caspase-Independent Pathway in Neuronal Death After Subarachnoid Hemorrhage in Mice. In: Martin, R., Boling, W., Chen, G., Zhang, J. (eds) Subarachnoid Hemorrhage. Acta Neurochirurgica Supplement, vol 127. Springer, Cham. https://doi.org/10.1007/978-3-030-04615-6_7
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DOI: https://doi.org/10.1007/978-3-030-04615-6_7
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