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Possible Involvement of Caspase-Independent Pathway in Neuronal Death After Subarachnoid Hemorrhage in Mice

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Subarachnoid Hemorrhage

Part of the book series: Acta Neurochirurgica Supplement ((NEUROCHIRURGICA,volume 127))

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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References

  1. Cahill J, Calvert JW, Zhang JH. Mechanisms of early brain injury after subarachnoid hemorrhage. J Cereb Blood Flow Metab. 2006;26:1341–53.

    Article  CAS  Google Scholar 

  2. Cregan SP, Fortin A, MacLaurin JG, Callaghan SM, Cecconi F, Yu SW, Dawson TM, Dawson VL, Park DS, Kroemer G, Slack RS. Apoptosis-inducing factor is involved in the regulation of caspase-independent neuronal cell death. J Cell Biol. 2002;158:507–17.

    Article  CAS  Google Scholar 

  3. Elmore S. Apoptosis: a review of programmed cell death. Toxicol Pathol. 2007;35:495–516.

    Article  CAS  Google Scholar 

  4. Li M, Wang W, Mai H, Zhang X, Wang J, Gao Y, Wang Y, Deng G, Gao L, Zhou S, Chen Q, Wang X. Methazolamide improves neurological behavior by inhibition of neuron apoptosis in subarachnoid hemorrhage in mice. Sci Rep. 2016;6:35055.

    Article  CAS  Google Scholar 

  5. Mcllwain DR, Berger T, Mak TW. Caspase functions in cell death and disease. Cold Spring Harb Perspect Biol. 2013;5:a008656.

    Google Scholar 

  6. Northington FJ, Zelaya ME, O’Riordan DP, Blomgren K, Flock DL, Hagberg H, Ferriero DM, Martin LJ. Failure to complete apoptosis following neonatal hypoxia-ischemia manifests as “continuum” phenotype of cell death and occurs with multiple manifestations of mitochondrial dysfunction in rodent forebrain. Neuroscience. 2007;149:822–33.

    Article  CAS  Google Scholar 

  7. Park S, Yamaguchi M, Zhou C, Calvert JW, Tang J, Zhang JH. Neurovascular protection reduces early brain injury after subarachnoid hemorrhage. Stroke. 2004;35:2412–7.

    Article  CAS  Google Scholar 

  8. Shiba M, Fujimoto M, Imanaka-Yoshida K, Yoshida T, Taki W, Suzuki H. Tenascin-C causes neuronal apoptosis after subarachnoid hemorrhage in rats. Transl Stroke Res. 2014;5:238–47.

    Article  Google Scholar 

  9. Tait SW, Green DR. Caspase-independent cell death: leaving the set without the final cut. Oncogene. 2008;27:6452–61.

    Article  CAS  Google Scholar 

  10. Wang B, Armstrong JS, Lee JH, Bhalala U, Kulikowicz E, Zhang H, Reyes M, Moy N, Spicer D, Zhu J, Yang ZJ, Koehler RC, Martin LJ, Lee JK. Rewarming from therapeutic hypothermia induces cortical neuron apoptosis in a swine model of neonatal hypoxic-ischemic encephalopathy. J Cereb Blood Flow Metab. 2015;35:781–93.

    Article  Google Scholar 

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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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Correspondence to Fumi Nakano .

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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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  • Publisher Name: Springer, Cham

  • Print ISBN: 978-3-030-04614-9

  • Online ISBN: 978-3-030-04615-6

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