alexa Oxidative stress activates STAT1 in basilar arteries after subarachnoid hemorrhage.
Psychiatry

Psychiatry

Journal of Addiction Research & Therapy

Author(s): Osuka K, Watanabe Y, Usuda N, Atsuzawa K, Wakabayashi T,

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Abstract The signal transducer and activator of transcription 1 (STAT1) is one of the most important signaling molecule transducing signals from the cell surface in response to cytokines or growth factors. Subarachnoid hemorrhage (SAH) results in production of cytokines and growth factors in the CSF. We here investigated whether this signaling molecule is activated in the rat basilar artery after SAH. In a rat single-hemorrhage model of SAH, basilar arteries were obtained at various times until 7days after SAH. Western blot analysis with phosphorylated (p)-STAT1 at Tyr(701), p-STAT1 at Ser(727), STAT1, and actin antibodies was performed. The expression of STAT1 and p-STAT1 at Tyr(701) in basilar arteries was also examined by immunohistochemistry. Intracisternal injection of interleukin-6 (IL-6), hydrogen peroxide, or hydroxyl radical scavenger was conducted to examine for phosphorylation of STAT1. Western blot analysis showed STAT1 to be significantly phosphorylated at Tyr(701) and Ser(727) within 2h of SAH and to gradually decrease thereafter. Immunohistochemistry revealed this phosphorylation of STAT1 to occur in the outer membranes of the basilar artery. Intracisternal injection of hydrogen peroxide, but not IL-6, also significantly increased phosphorylation of STAT1 at Tyr(701). Hydroxyl radical scavenger significantly reduced phosphorylation of STAT1. These results indicate that reactive oxygen species, produced in the CSF after SAH, activates STAT1 molecule in the outer membranes of basilar arteries. This STAT1 signaling might contribute to morphological arterial wall changes in cerebral vasospasm. Copyright 2010 Elsevier B.V. All rights reserved. This article was published in Brain Res and referenced in Journal of Addiction Research & Therapy

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