KMID : 0380020130280040230
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Korean Journal of Biotechnology and Bioengineering 2013 Volume.28 No. 4 p.230 ~ p.237
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Effects Amyloid Beta Peptide on the Inflammatory Response in Neuronal Cells
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Jang Seon-A
Koo Hyun-Jung Kang Se-Chan Sohn Eun-Hwa Namkoong Seung
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Abstract
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Amyloid ¥â peptide (A¥â) still best known as a molecule to cause Alzheimer's disease (AD). AD is characterized by the accumulation and deposition of A¥â within the brain, leading to neuronal cell loss and perturbation of synaptic function by causing free radical formation, inflammation and apoptosis. We investigated the inflammatory action of A¥â on two types of brain cells, neuronal cells (SH-SY5Y) and neuroglia cells (C6), and its mechanism. We measured the production of NO-iNOS, TNF-¥á, and ICAM-1 using RT-PCR and Western blot analysis less than the concentration of cytotoxic effects (> 70% survivability). A¥â had no effect on the production of NO and TNF-¥á, but significantly increases of iNOS and ICAM-1. Based on this, we suggest that the inflammatory effect of A¥â results from the action of ICAM-1 in neuronal cells, rather than the release of inflammatory mediators such as NO and TNF-¥á in neuroglia cells. In addition, we confirmed whether p53 was related to the action of A¥â by using SH-SY5Y (p53-/-) dominant cells. Neither the expression of p53 nor the cytotoxicity of SH-SY5Y (p53-/-) cells were directly affected by A¥â. However, ICAM-1 was not expressed in SH-SY5Y (p53-/-) cells. This means that p53-independent pathway exists in the expression of ICAM-1 by A¥â while p53 plays a role as an on-and-off switch.
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KEYWORD
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Amyloid ¥â peptide, SH-SY5Y, C6, ICAM-1, p53
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