• 대한의생명과학회지
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• 제21권3호
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• pp.160-163
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• 2015

The effects of hypothermic treatment ($32^{\circ}C$) on recovery from ischemia are controversial because the precise mechanisms of hypothermia remain unclear. We demonstrated previously that hypothermia induces beta-catenin-interacting protein 1 (CTNNBIP1) gene expression in vitro. In this study, we evaluated the effects of various hypothermic conditions, including lithium chloride treatment, on CTNNBIP1 gene expression. The results show that short-term hypothermic treatment resulted in relatively higher CTNNBIP1 gene expression than that of a longer treatment. These findings indicate that hypothermia controls CTNNBIP1 gene expression, which may provide clues to develop treatments to recover from and diagnose ischemia.

• 대한의생명과학회지
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• 제20권3호
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• pp.168-172
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• 2014

It has recently been shown that hypothermia treatment improves brain ischemia injury and is being increasingly considered by many clinicians. However, the precise roles of hypothermia for brain ischemia are not yet clear. In the present study we demonstrated firstly that hypothermia induced beta-catenin-interacting protein 1 (CTNNBIP1) gene expression and its expression was dramatically decreased under ischemic conditions. It was also demonstrated that hypothermia activated endoplasmic reticulum (ER) stress sensors especially both, the phosphorylation of $eIF2{\alpha}$, and ATF6 proteolytic cleavage. However, the factors of apoptosis and autophagy were not associated with hypothermia. These findings suggested that hypothermia controlled CTNNBIP1 gene expression under ischemia, which may provide a clue to the development of treatments and diagnostic methods for brain ischemia.