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

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초록

Thioredoxin-like protein 1 (TXNL1), one of the thioredoxin superfamilyknown as redox-regulator, plays an essential in maintainingcell survival via various antioxidant and anti-apoptoticmechanisms. It is well known that relationship between ischemiaand oxidative stress, however, the role of TXNL1 protein inischemic damage has not been fully investigated. In the presentstudy, we aimed to determine the protective role of TXNL1against on ischemic injury in vitro and in vivo using cellpermeable Tat-TXNL1 fusion protein. Transduced Tat-TXNL1inhibited ROS production and cell death in H2O2-exposedhippocampal neuronal (HT-22) cells and modulated MAPKsand Akt activation, and pro-apoptotic protein expression levelsin the cells. In an ischemia animal model, Tat-TXNL1 markedlydecreased hippocampal neuronal cell death and the activationof astrocytes and microglia. These findings indicate thatcell permeable Tat-TXNL1 protects against oxidative stress invitro and in vivo ischemic animal model. Therefore, we suggestTat-TXNL1 can be a potential therapeutic protein for ischemicinjury.

Abstract

Thioredoxin-like protein 1 (TXNL1), one of the thioredoxin superfamilyknown as redox-regulator, plays an essential in maintainingcell survival via various antioxidant and anti-apoptoticmechanisms. It is well known that relationship between ischemiaand oxidative stress, however, the role of TXNL1 protein inischemic damage has not been fully investigated. In the presentstudy, we aimed to determine the protective role of TXNL1against on ischemic injury in vitro and in vivo using cellpermeable Tat-TXNL1 fusion protein. Transduced Tat-TXNL1inhibited ROS production and cell death in H2O2-exposedhippocampal neuronal (HT-22) cells and modulated MAPKsand Akt activation, and pro-apoptotic protein expression levelsin the cells. In an ischemia animal model, Tat-TXNL1 markedlydecreased hippocampal neuronal cell death and the activationof astrocytes and microglia. These findings indicate thatcell permeable Tat-TXNL1 protects against oxidative stress invitro and in vivo ischemic animal model. Therefore, we suggestTat-TXNL1 can be a potential therapeutic protein for ischemicinjury.

참고문헌 (61)

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