NF-kappaB p50 is increased in neurons surviving hippocampal injury.

Signal transduction pathways that lead to the modulation of genes related to survival and repair mechanisms are activated in neurons that survive injury. These protein kinase/phosphatase cascades converge on transcription factors, the DNA binding proteins that directly regulate gene expression. In this study we examined expression of the NF-kappaB p50 subunit in the rat hippocampus 7 days after injury caused by middle cerebral artery occlusion or trimethyltin treatment.

Nicotine inhibition of apoptosis in murine immune cells.

Nicotine, the addictive component of tobacco, is thought to be at least partially responsible for the deleterious effects of smoking such as heart disease and cancer. Evidence shows that nicotine is an immunomodulator and that one of its possible mechanisms is regulation of apoptosis, or programmed cell death, in immune cells. This study examined the effects and the mechanisms of action of nicotine on dexamethasone (DEX)-induced apoptosis in murine immune cells by examining the expression of levels of the 17-kDa active caspase-3, a marker of apoptosis.

Brain injury: prolonged induction of transcription factors.

A specific temporal order of events at the cellular and molecular level occurs in response to injury to the brain. Injury-compromised neurons degenerate while surviving neurons undergo neuritogenesis and synaptogenesis to establish neuronal connectivity destroyed in the injury. Several genes, such as those coding cytoskeletal proteins and growth factors, have been shown to be regulated by AP-1 and NF-kappa B transcription factors, two of the most studied DNA binding regulatory proteins.

Expression of fos-related antigen-2 in rat hippocampus after middle cerebral arterial occlusion.

AP-1 transcription factors have been shown to be induced in the brain after ischemic injury. However, their roles in neuronal survival or death have yet to be defined. Here, we report the discovery of elevated nuclear levels of fos-related antigen-2 (FRA-2) in the nuclei of hippocampal neurons seven days after middle cerebral artery occlusion (MCAO).