Teoh, Jonathan and Boulos, Sherif and Chieng, Joanne and Knuckey, Neville W. and Meloni, Bruno P. (2014) Over-Expressing Prohibitin (PHB) in Neuronal Cultures Exacerbates Cell Death Following Hydrogen Peroxide and L-Glutamic Acid Induced Injury. Neuroscience and Medicine, 05 (04). pp. 149-160. ISSN 2158-2912
![[thumbnail of NM_2014090113473947.pdf]](http://publish7promo.com/style/images/fileicons/text.png)
NM_2014090113473947.pdf - Published Version
Download (2MB)
Abstract
Using proteomics, previous work in our laboratory identified five mitochondrial related proteins [citrate synthase (CS), glucose-regulated protein 75 (GRP75), heat shock protein 60 (HSP60), prohibitin (PHB), voltage-dependent anion channel 1 (VDAC1)] to be differentially expressed in primary cortical neuronal cultures following preconditioning treatments [1] [2]. To investigate a protective or damaging role of these five proteins in neurons, we used RNAi constructs to knockdown and adenoviral vectors to over-express the proteins in cortical neuronal cultures prior to exposure to three ischemia-related injury models: excitotoxicity (L-glutamic acid), oxidative stress (hydrogen peroxide) and in vitro ischemia (oxygen-glucose deprivation). We observed that down-regulating these mitochondrial proteins had no effect on neuronal viability, in any injury model. By contrast, over-expression of PHB exacerbated cell death in the hydrogen peroxide and L-glutamic acid injury models. These findings indicate that PHB plays a neurodamaging role following oxidative and excitotoxic stress and suggests that the protein is a potential therapeutic target for the design of drugs to limit neuronal death following cerebral ischemia and other forms of brain injury.
Item Type: | Article |
---|---|
Subjects: | Euro Archives > Medical Science |
Depositing User: | Managing Editor |
Date Deposited: | 10 Feb 2023 05:14 |
Last Modified: | 07 Feb 2024 04:11 |
URI: | http://publish7promo.com/id/eprint/1876 |