RGD Reference Report - NGF stimulation increases JNK2 phosphorylation and reduces caspase-3 activity in the olfactory bulb of estrogen-replaced animals. - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

NGF stimulation increases JNK2 phosphorylation and reduces caspase-3 activity in the olfactory bulb of estrogen-replaced animals.

Authors: Jezierski, MK  Sturm, AK  Scarborough, MM  Sohrabji, F 
Citation: Jezierski MK, etal., Endocrinology. 2001 Jun;142(6):2401.
RGD ID: 10412693
Pubmed: PMID:11356687   (View Abstract at PubMed)
DOI: DOI:10.1210/endo.142.6.8316   (Journal Full-text)

Estrogen receptors are extensively colocalized with neurotrophins and their receptors in the rodent forebrain. We have shown previously that estrogen increases mRNA and protein expression of the nerve growth factor (NGF)-specific tyrosine kinase receptor, trkA, while decreasing expression of the universal neurotrophin receptor p75. In view of the pro-survival roles described for trks and the context-dependent stimulation of survival and cell death pathways activated by p75, differential regulation of these receptors by estrogen is likely to alter neurotrophin-dependent cell signaling. This hypothesis was tested in vivo, using the rodent olfactory bulb as a model. We found that NGF activated the extracellular signal-regulated protein kinase (ERK) equally in estrogen replaced and hormone-deprived animals. However in the case of c-jun-kinase (JNK), a related MAP kinase, pretreatment with estrogen altered NGF activation of a specific isoform of this protein. Specifically, NGF stimulation did not alter JNK1 or JNK2 activation in the estrogen-deprived condition, but significantly increased JNK2 activation in estrogen-replaced animals. Increased JNK2 phosphorylation in the NGF-injected, estrogen- replaced animals was paralleled by decreased activity of caspase-3, an enzyme required for apoptosis. In view of the disparate roles assigned to JNK, this latter finding suggests that estrogen pretreatment may preferentially direct neurotrophin-dependent JNK activation toward regeneration and plasticity rather than cell death.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
response to nerve growth factor  IEP 10412693 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Mapk9  (mitogen-activated protein kinase 9)


Additional Information