| Title: |
The lipid peroxidation product 4-hydroxy-2,3-nonenal inhibits constitutive and inducible activity of nuclear factor kappa B in neurons. |
| Authors: |
CAMANDOLA S.; MATTSON MP; POLI, Giuseppe |
| Contributors: |
CAMANDOLA S; POLI G; MATTSON MP |
| Publication Year: |
2000 |
| Collection: |
Università degli studi di Torino: AperTo (Archivio Istituzionale ad Accesso Aperto) |
| Description: |
Peroxidation of membrane lipids occurs in many different neurodegenerative conditions including stroke, and Alzheimer's and Parkinson's diseases. Recent findings suggest that lipid peroxidation can promote neuronal death by a mechanism involving production of the toxic aldehyde 4-hydroxy-2,3-nonenal (HNE), which may act by covalently modifying proteins and impairing their function. The transcription factor NF-kappa B can prevent neuronal death in experimental models of neurodegenerative disorders by inducing the expression of anti-apoptotic proteins including Bcl-2 and manganese superoxide dismutase. We now report that HNE selectively suppresses basal and inducible NF-kappa B DNA binding activity in cultured rat cortical neurons. Immunoprecipitation-immunoblot analyses using antibodies against HNE-conjugated proteins and p50 and p65 NF-kappa B subunits indicate that HNE does not directly modify NF-kappa B proteins. Moreover, HNE did not affect NF-kappa B DNA-binding activity when added directly to cytosolic extracts, suggesting that HNE inhibits an upstream component of the NF-kappa B signaling pathway. Inhibition of the survival-promoting NF-kappa B signaling pathway by HNE may contribute to neuronal death under conditions in which membrane lipid peroxidation occurs. |
| Document Type: |
article in journal/newspaper |
| Language: |
English |
| Relation: |
info:eu-repo/semantics/altIdentifier/pmid/11146106; volume:85; firstpage:53; lastpage:60; journal:MOLECULAR BRAIN RESEARCH; http://hdl.handle.net/2318/33985 |
| Availability: |
http://hdl.handle.net/2318/33985 |
| Accession Number: |
edsbas.4DEA7931 |
| Database: |
BASE |