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Effect of prothymosin α on neuroplasticity following cerebral ischemia‑reperfusion injury

  • Authors:
    • Ai-Chiang Lee
    • Shih-Huang Tai
    • Yi-Yun Chen
    • Sheng-Yang Huang
    • Chao-Liang Wu
    • E-Jian Lee
  • View Affiliations / Copyright

    Affiliations: Neurophysiology Laboratory, Neurosurgical Service, Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan 70428, Taiwan, R.O.C., Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan, R.O.C.
    Copyright: © Lee et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 59
    |
    Published online on: February 16, 2024
       https://doi.org/10.3892/mmr.2024.13183
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Abstract

Prothymosin α (ProT), a highly acidic nuclear protein with multiple cellular functions, has shown potential neuroprotective properties attributed to its anti‑necrotic and anti‑apoptotic activities. The present study aimed to investigate the beneficial effect of ProT on neuroplasticity after ischemia‑reperfusion injury and elucidate its underlying mechanism of action. Primary cortical neurons were either treated with ProT or overexpressing ProT by gene transfection and exposed to oxygen‑glucose deprivation for 2 h in vitro. Immunofluorescence staining for ProT and MAP‑2 was performed to quantify ProT protein expression and assess neuronal arborization. Mice treated with vehicle or ProT (100 µg/kg) and ProT overexpression in transgenic mice received middle cerebral artery occlusion for 50 min to evaluate the effect of ProT on neuroplasticity‑associated protein following ischemia‑reperfusion injury. The results demonstrated that in cultured neurons ProT significantly increased neurite lengths and the number of branches, accompanied by an upregulation mRNA level of brain‑derived neurotrophic factor. Furthermore, ProT administration improved the protein expressions of synaptosomal‑associated protein, 25 kDa and postsynaptic density protein 95 after ischemic‑reperfusion injury in vivo. These findings suggested that ProT can potentially induce neuroplasticity effects following ischemia‑reperfusion injury.
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Copy and paste a formatted citation
Spandidos Publications style
Lee A, Tai S, Chen Y, Huang S, Wu C and Lee E: Effect of prothymosin α on neuroplasticity following cerebral ischemia‑reperfusion injury. Mol Med Rep 29: 59, 2024.
APA
Lee, A., Tai, S., Chen, Y., Huang, S., Wu, C., & Lee, E. (2024). Effect of prothymosin α on neuroplasticity following cerebral ischemia‑reperfusion injury. Molecular Medicine Reports, 29, 59. https://doi.org/10.3892/mmr.2024.13183
MLA
Lee, A., Tai, S., Chen, Y., Huang, S., Wu, C., Lee, E."Effect of prothymosin α on neuroplasticity following cerebral ischemia‑reperfusion injury". Molecular Medicine Reports 29.4 (2024): 59.
Chicago
Lee, A., Tai, S., Chen, Y., Huang, S., Wu, C., Lee, E."Effect of prothymosin α on neuroplasticity following cerebral ischemia‑reperfusion injury". Molecular Medicine Reports 29, no. 4 (2024): 59. https://doi.org/10.3892/mmr.2024.13183
Copy and paste a formatted citation
x
Spandidos Publications style
Lee A, Tai S, Chen Y, Huang S, Wu C and Lee E: Effect of prothymosin α on neuroplasticity following cerebral ischemia‑reperfusion injury. Mol Med Rep 29: 59, 2024.
APA
Lee, A., Tai, S., Chen, Y., Huang, S., Wu, C., & Lee, E. (2024). Effect of prothymosin α on neuroplasticity following cerebral ischemia‑reperfusion injury. Molecular Medicine Reports, 29, 59. https://doi.org/10.3892/mmr.2024.13183
MLA
Lee, A., Tai, S., Chen, Y., Huang, S., Wu, C., Lee, E."Effect of prothymosin α on neuroplasticity following cerebral ischemia‑reperfusion injury". Molecular Medicine Reports 29.4 (2024): 59.
Chicago
Lee, A., Tai, S., Chen, Y., Huang, S., Wu, C., Lee, E."Effect of prothymosin α on neuroplasticity following cerebral ischemia‑reperfusion injury". Molecular Medicine Reports 29, no. 4 (2024): 59. https://doi.org/10.3892/mmr.2024.13183
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