Notch1 inhibits neurite outgrowth in postmitotic primary neurons

Berezovska, Oksana; McLean, Pamela J.; Knowles, Roger B.; Frosh, M.; Lu, Frederick M.; Lux, Samuel E.; Hyman, Bradley T.

doi:10.1016/s0306-4522(99)00157-8

Cited by 208 publications

(170 citation statements)

References 44 publications

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“…Indeed, we have found the regulation of three members of the Notch pathway, namely deltex homolog 3, embryonal stem cell specific gene 1 and dickkopf 2. Given the involvement of this pathway in cell fate and differentiation and in the regulation of neurite growth and adult neurogenesis (Berezovska et al, 1999;Costa et al, 2005), it is likely that these genes participate in the synaptic morphological changes induced by EE in the striatum (Comery et al, 1996;Kolb et al, 2003a,b). EE down-regulated the expression of several other genes that encode for proteins involved in cell structure such as synaptotagmin-like 4, Actinin alpha 3, Decorin, Actin alpha 2.…”

Section: Discussionmentioning

confidence: 99%

Environmental enrichment during adolescence regulates gene expression in the striatum of mice

et al. 2008

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We have previously shown that environmental enrichment decreases the activating and rewarding effects of the psych psychostimulant cocaine and increases resistance to the neurotoxic effect of the Parkinson-inducing drug MPTP. These effects were accompanied by an increase in the striatal expression of the neurotrophin BDNF, an increase in the striatal levels of delta-Fos B and by a decrease in striatal levels of the dopamine transporter, the main molecular target for cocaine and MPTP. Here, we used cDNA arrays to investigate the effects of rearing mice in enriched environments from weaning to adulthood on the profile of expression of genes in the striatum focusing on genes involved in intracellular signalling and functioning. We found that mice reared in an enriched environment show several alterations in the levels of mRNA coding for proteins involved in cell proliferation, cell differentiation, signal transduction, transcription and translation, cell structure and meta metabolism. Several of these findings were further confirmed by real-time quantitative PCR and, in the case of protein kinase C lambda, also by western blot. These findings are the first description of alterations in striatal gene expression by an enriched environment. The striatal gene expression regulation by environment that we report here may play a role in the resistance to the effects of drugs of abuse and dopaminergic neurotoxins previously reported.

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Section: Discussionmentioning

confidence: 99%

Environmental enrichment during adolescence regulates gene expression in the striatum of mice

et al. 2008

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“…Primary neuronal cultures were prepared as described by Berezovska et al (10). In brief, cells were isolated from neocortex of embryonic day 16 -17 normal and transgenic mice and placed in Neurobasal medium (Life Technologies) with 10% FBS.…”

Section: Cortical Cell Cultures Experimental Treatments and Quantifmentioning

confidence: 99%

Inflammatory Response and Glutathione Peroxidase in a Model of Stroke

Ishibashi

Prokopenko

Reuhl

et al. 2002

The Journal of Immunology

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Stroke is one of the leading causes of death in major industrial countries. Many factors contribute to the cellular damage resulting from ischemia/reperfusion (I/R). Experimental data indicate an important role for oxidative stress and the inflammatory cascade during I/R. We are testing the hypothesis that the mechanism of protection against I/R damage observed in transgenic mice overexpressing human antioxidant enzymes (particularly intracellular glutathione peroxidase) involves the modulation of inflammatory response as well as reduced sensitivity of neurons to cytotoxic cytokines. Transgenic animals show significant reduction of expression of chemokines, IL-6, and cell death-inducing ligands as well as corresponding receptors in a focal cerebral I/R model. Reduction of DNA binding activity of consensus and potential AP-1 binding sites in mouse Fas ligand promoter sequence was observed in nuclear extracts from transgenic mice overexpressing intracellular glutathione peroxidase compared with normal animals following I/R. This effect was accompanied by modulation of the c-Jun N-terminal kinase/stress-activated protein kinase pathway. Cultured primary neurons from the transgenic mice demonstrated protection against hypoxia/reoxygenation injury as well as cytotoxicity after TNF-α and Fas ligand treatment. These results indicate that glutathione peroxidase-sensitive reactive oxygen species play an important role in regulation of cell death during cerebral I/R by modulating intrinsic neuronal sensitivity as well as brain inflammatory reactions.

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“…There is strong evidence that Notch signaling participates in mammalian brain development, primarily inhibiting neuronal differentiation and allowing/ promoting glial differentiation (Morrison et al, 2000;Grandbarbe et al, 2003). Expression of Notch in the adult brain has been described (Berezovska et al, 1998;Berezovska et al, 1999), but the postnatal neurological functions of Notch signaling remain largely unexplored.…”

Section: Other Organs and Tissuesmentioning

confidence: 99%