The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Uterotrophic actions of estradiol and tamoxifen are associated with inhibition of uterine insulin-like growth factor binding protein 3 gene expression.

We have recently shown that uterine insulin-like growth factor I (IGF-I) gene expression is up-regulated by tamoxifen, a uterotrophic partial antagonist to the estrogen receptor, but down-regulated by the complete estrogen receptor antagonist ICI 182780, which causes uterine involution. This result is consistent with prior reports indicating that the uterotrophic effects of estradiol are mediated at least in part by estradiol-stimulated uterine IGF-I gene expression. We demonstrate here that the uterotrophic agents estradiol and tamoxifen each suppress expression of the IGF binding protein 3 (IGFBP-3) gene in uterus to less than one-third of control values, while oophorectomy or administration of the complete estrogen receptor antagonist ICI 182780, both of which result in uterine involution, are associated with a greater than 3-fold stimulation of uterine IGFBP-3 gene expression. The data reveal a negative correlation between uterine weight and uterine IGFBP-3 gene expression as well as reciprocal regulation by estradiol of expression in uterus of the genes encoding IGF-I and IGFBP-3. In vitro, IGFBP-3 protein accumulation in media conditioned by primary uterine cultures was decreased by estradiol treatment and increased by ICI 182780 treatment. Together, these observations provide a novel mechanism by which estradiol and antiestrogens modulate uterine IGF-I physiology that is consistent with the view that the mitogenic activity of IGF-I is reduced in the presence of IGFBP-3. The uterotrophic toxicity of chronic estradiol or tamoxifen treatment may be causally related to both the inhibition of uterine IGFBP-3 expression and the stimulation of uterine IGF-I expression by these compounds.[1]

References

 
WikiGenes - Universities