Transient Receptor Potential Mucolipin-1 Participates in Intracerebral Hemorrhage-Induced Secondary Brain Injury by Inducing Neuroinflammation and Neuronal Cell Death

doi:10.1007/s12017-023-08734-5

. 2023 Jun;25(2):272-285.

doi: 10.1007/s12017-023-08734-5. Epub 2023 Feb 4.

Transient Receptor Potential Mucolipin-1 Participates in Intracerebral Hemorrhage-Induced Secondary Brain Injury by Inducing Neuroinflammation and Neuronal Cell Death

Jinzhao Shi^#¹, Xiang Li^#^{2

3}, Jiasheng Ding^{2

3}, Jinrong Lian^{2

3}, Yi Zhong^{2

3}, Haiying Li^{2

3}, Haitao Shen^{2

3}, Wanchun You^{4

5}, Xi'an Fu⁶, Gang Chen^{2

3}

Affiliations

¹ Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, 215008, Jiangsu Province, China.
² Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, Jiangsu Province, China.
³ Institute of Stroke Research, Soochow University, Suzhou, 215006, Jiangsu Province, China.
⁴ Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, Jiangsu Province, China. wcyou@suda.edu.cn.
⁵ Institute of Stroke Research, Soochow University, Suzhou, 215006, Jiangsu Province, China. wcyou@suda.edu.cn.
⁶ Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, 215008, Jiangsu Province, China. cowankang@126.com.

^# Contributed equally.

PMID: 36737508
DOI: 10.1007/s12017-023-08734-5

Transient Receptor Potential Mucolipin-1 Participates in Intracerebral Hemorrhage-Induced Secondary Brain Injury by Inducing Neuroinflammation and Neuronal Cell Death

Jinzhao Shi et al. Neuromolecular Med. 2023 Jun.

. 2023 Jun;25(2):272-285.

doi: 10.1007/s12017-023-08734-5. Epub 2023 Feb 4.

Authors

Jinzhao Shi^#¹, Xiang Li^#^{2

3}, Jiasheng Ding^{2

3}, Jinrong Lian^{2

3}, Yi Zhong^{2

3}, Haiying Li^{2

3}, Haitao Shen^{2

3}, Wanchun You^{4

5}, Xi'an Fu⁶, Gang Chen^{2

3}

Affiliations

¹ Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, 215008, Jiangsu Province, China.
² Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, Jiangsu Province, China.
³ Institute of Stroke Research, Soochow University, Suzhou, 215006, Jiangsu Province, China.
⁴ Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, Jiangsu Province, China. wcyou@suda.edu.cn.
⁵ Institute of Stroke Research, Soochow University, Suzhou, 215006, Jiangsu Province, China. wcyou@suda.edu.cn.
⁶ Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, 215008, Jiangsu Province, China. cowankang@126.com.

^# Contributed equally.

PMID: 36737508
DOI: 10.1007/s12017-023-08734-5

Abstract

Transient receptor potential mucolipin-1 (TRPML1) is the most abundantly and widely expressed channel protein in the TRP family. While numerous studies have been conducted involving many aspects of TRPML1, such as its role in cell biology, oncology, and neurodegenerative diseases, there are limited reports about what role it plays in intracerebral hemorrhage (ICH)-induced secondary brain injury (SBI). Here we examined the function of TRPML1 in ICH-induced SBI. The caudal arterial blood of rats was injected into the caudate nucleus of basal ganglia to establish an experimental ICH model. We observed that lentivirus downregulated the expression level of TRPML1 and chemical agonist promoted the enzyme activity of TRPML1. The results indicated that the protein levels of TRPML1 in brain tissues increased 24 h after ICH. These results suggested that downregulated TRPML1 could significantly reduce inflammatory cytokines, and ICH induced the production of LDH and ROS. Furthermore, TRPML1 knockout relieved ICH-induced neuronal cell death and degeneration, and declines in learning and memory after ICH could be improved by downregulating the expression of TRPML1. In addition, chemical agonist-expressed TRPML1 showed the opposite effect and exacerbated SBI after ICH. In summary, this study demonstrated that TRPML1 contributed to brain injury after ICH, and downregulating TRPML1 could improve ICH-induced SBI, suggesting a potential target for ICH therapy.

Keywords: Intracerebral hemorrhage; Neuroinflammation; Neuronal cell death; Secondary brain injury; TRPML1.

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References

1. Baker, W. B., Balu, R., He, L., Kavuri, V. C., Busch, D. R., Amendolia, O., et al. (2019). Continuous non-invasive optical monitoring of cerebral blood flow and oxidative metabolism after acute brain injury. Journal of Cerebral Blood Flow and Metabolism, 39(8), 1469–1485. https://doi.org/10.1177/0271678x19846657 - DOI - PubMed - PMC
1. Bassi, M. T., Manzoni, M., Monti, E., Pizzo, M. T., Ballabio, A., & Borsani, G. (2000). Cloning of the gene encoding a novel integral membrane protein, mucolipidin-and identification of the two major founder mutations causing mucolipidosis type IV. American Journal of Human Genetics, 67(5), 1110–1120. https://doi.org/10.1016/s0002-9297(07)62941-3 - DOI - PubMed - PMC
1. Bobinger, T., Burkardt, P., Huttner, H. B., & Manaenko, A. (2018). Programmed cell death after intracerebral hemorrhage. Current Neuropharmacology, 16(9), 1267–1281. https://doi.org/10.2174/1570159x15666170602112851 - DOI - PubMed - PMC
1. Bogorad, M., DeStefano, J., Linville, R., Wong, A., & Searson, P. (2019). Cerebrovascular plasticity: Processes that lead to changes in the architecture of brain microvessels. Journal of Cerebral Blood Flow & Metabolism, 39(8), 1413–1432. https://doi.org/10.1177/0271678x19855875 - DOI
1. Carrillo-Jimenez, A., Deniz, Ö., Niklison-Chirou, M. V., Ruiz, R., Bezerra-Salomão, K., Stratoulias, V., Amouroux, R., Yip, P. K., Vilalta, A., Cheray, M., & Scott-Egerton, A. M. (2019). TET2 regulates the neuroinflammatory response in microglia. Cell Reports, 29(3), 697-713.e698. https://doi.org/10.1016/j.celrep.2019.09.013 - DOI - PubMed

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[1] Baker, W. B., Balu, R., He, L., Kavuri, V. C., Busch, D. R., Amendolia, O., et al. (2019). Continuous non-invasive optical monitoring of cerebral blood flow and oxidative metabolism after acute brain injury. Journal of Cerebral Blood Flow and Metabolism, 39(8), 1469–1485. https://doi.org/10.1177/0271678x19846657 - DOI - PubMed - PMC

[2] Baker, W. B., Balu, R., He, L., Kavuri, V. C., Busch, D. R., Amendolia, O., et al. (2019). Continuous non-invasive optical monitoring of cerebral blood flow and oxidative metabolism after acute brain injury. Journal of Cerebral Blood Flow and Metabolism, 39(8), 1469–1485. https://doi.org/10.1177/0271678x19846657 - DOI - PubMed - PMC

[3] Bassi, M. T., Manzoni, M., Monti, E., Pizzo, M. T., Ballabio, A., & Borsani, G. (2000). Cloning of the gene encoding a novel integral membrane protein, mucolipidin-and identification of the two major founder mutations causing mucolipidosis type IV. American Journal of Human Genetics, 67(5), 1110–1120. https://doi.org/10.1016/s0002-9297(07)62941-3 - DOI - PubMed - PMC

[4] Bassi, M. T., Manzoni, M., Monti, E., Pizzo, M. T., Ballabio, A., & Borsani, G. (2000). Cloning of the gene encoding a novel integral membrane protein, mucolipidin-and identification of the two major founder mutations causing mucolipidosis type IV. American Journal of Human Genetics, 67(5), 1110–1120. https://doi.org/10.1016/s0002-9297(07)62941-3 - DOI - PubMed - PMC

[5] Bobinger, T., Burkardt, P., Huttner, H. B., & Manaenko, A. (2018). Programmed cell death after intracerebral hemorrhage. Current Neuropharmacology, 16(9), 1267–1281. https://doi.org/10.2174/1570159x15666170602112851 - DOI - PubMed - PMC

[6] Bobinger, T., Burkardt, P., Huttner, H. B., & Manaenko, A. (2018). Programmed cell death after intracerebral hemorrhage. Current Neuropharmacology, 16(9), 1267–1281. https://doi.org/10.2174/1570159x15666170602112851 - DOI - PubMed - PMC

[7] Bogorad, M., DeStefano, J., Linville, R., Wong, A., & Searson, P. (2019). Cerebrovascular plasticity: Processes that lead to changes in the architecture of brain microvessels. Journal of Cerebral Blood Flow & Metabolism, 39(8), 1413–1432. https://doi.org/10.1177/0271678x19855875 - DOI

[8] Bogorad, M., DeStefano, J., Linville, R., Wong, A., & Searson, P. (2019). Cerebrovascular plasticity: Processes that lead to changes in the architecture of brain microvessels. Journal of Cerebral Blood Flow & Metabolism, 39(8), 1413–1432. https://doi.org/10.1177/0271678x19855875 - DOI

[9] Carrillo-Jimenez, A., Deniz, Ö., Niklison-Chirou, M. V., Ruiz, R., Bezerra-Salomão, K., Stratoulias, V., Amouroux, R., Yip, P. K., Vilalta, A., Cheray, M., & Scott-Egerton, A. M. (2019). TET2 regulates the neuroinflammatory response in microglia. Cell Reports, 29(3), 697-713.e698. https://doi.org/10.1016/j.celrep.2019.09.013 - DOI - PubMed

[10] Carrillo-Jimenez, A., Deniz, Ö., Niklison-Chirou, M. V., Ruiz, R., Bezerra-Salomão, K., Stratoulias, V., Amouroux, R., Yip, P. K., Vilalta, A., Cheray, M., & Scott-Egerton, A. M. (2019). TET2 regulates the neuroinflammatory response in microglia. Cell Reports, 29(3), 697-713.e698. https://doi.org/10.1016/j.celrep.2019.09.013 - DOI - PubMed

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Transient Receptor Potential Mucolipin-1 Participates in Intracerebral Hemorrhage-Induced Secondary Brain Injury by Inducing Neuroinflammation and Neuronal Cell Death

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Transient Receptor Potential Mucolipin-1 Participates in Intracerebral Hemorrhage-Induced Secondary Brain Injury by Inducing Neuroinflammation and Neuronal Cell Death

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