Tat-Thioredoxin-like protein 1 attenuates ischemic brain injury by regulation of MAPKs and apoptosis signaling

BMB Rep. 2023 Apr;56(4):234-239. doi: 10.5483/BMBRep.2022-0184.

Abstract

Thioredoxin-like protein 1 (TXNL1), one of the thioredoxin superfamily known as redox-regulator, plays an essential in maintaining cell survival via various antioxidant and anti-apoptotic mechanisms. It is well known that relationship between ischemia and oxidative stress, however, the role of TXNL1 protein in ischemic damage has not been fully investigated. In the present study, we aimed to determine the protective role of TXNL1 against on ischemic injury in vitro and in vivo using cell permeable Tat-TXNL1 fusion protein. Transduced Tat-TXNL1 inhibited ROS production and cell death in H2O2-exposed hippocampal neuronal (HT-22) cells and modulated MAPKs and Akt activation, and pro-apoptotic protein expression levels in the cells. In an ischemia animal model, Tat-TXNL1 markedly decreased hippocampal neuronal cell death and the activation of astrocytes and microglia. These findings indicate that cell permeable Tat-TXNL1 protects against oxidative stress in vitro and in vivo ischemic animal model. Therefore, we suggest Tat-TXNL1 can be a potential therapeutic protein for ischemic injury. [BMB Reports 2023; 56(4): 234-239].

Publication types

  • News

MeSH terms

  • Animals
  • Apoptosis
  • Brain Injuries*
  • Cell Line
  • Gene Products, tat / metabolism
  • Hydrogen Peroxide* / pharmacology
  • Ischemia
  • Oxidative Stress
  • Recombinant Fusion Proteins / genetics
  • Recombinant Fusion Proteins / metabolism
  • Recombinant Fusion Proteins / pharmacology
  • Thioredoxins / genetics
  • Thioredoxins / metabolism

Substances

  • Hydrogen Peroxide
  • Gene Products, tat
  • Thioredoxins
  • Recombinant Fusion Proteins

Grants and funding

ACKNOWLEDGEMENTS This research was supported by Basic Science Research Program (2018R1D1A3B07049265 & 2019R1A6A1A11036849) through the National Research Foundation of Korea (NRF) funded by the Ministry of Education.