Sp1 increases its stability in neuronal cells under oxygen and glucose deprivation stress

• Main Authors: Chia-Wen Jeng, 鄭嘉文
• Other Authors: Wen-Chang Chang
• Format: Others
• Language: zh-TW
• Published: 2007
• Online Access: http://ndltd.ncl.edu.tw/handle/28839278700872112150

碩士 === 國立成功大學 === 藥理學研究所 === 95 === Sp1 is a ubiquitous transcription factor which is considered constitutively regulating numerous gene expressions. Previous investigation indicated that Sp1 DNA-binding activity is increased in hypoxia condition and regulate gene expression, such as COX-2 and VEGF. Recent studies said that increase pf Sp1 was evident at 1 h and was more prominent at 3 h after middle cerebral artery occlusion (MCAO), especially in large neuron-like cells. Apoptotic cell death pathways have also been implicated in ischemic cerebral injury in ischemia animal models. It is still not clear whether Sp1 plays any role in cerebral ischemia injury. Here, we use oxygen glucose deprivation (OGD) in primary culture as an in vitro ischemia model. We found that expression of Sp1 was increased in neuronal cells after OGD treatment, but not in glial cells. However, the Sp1 upregulation is mostly contributed to the hypoxia condition. The RT-PCR data indicated that the increasing of Sp1 does not due to transcriptional control. Furthermore, we use cycloheximide, which is a translational inhibitor, and discovered that the increase Sp1 protein expression after OGD is due to Sp1 protein stability increases. We also found that Sp1 increase play a positive role after OGD stress.