Nerve growth factor (NGF) and NGF mRNA change in rat uterus during pregnancy

Varol, Füsun; Duchemin, Anne‐Marie; Neff, Norton H.; Hadjiconstantinou, Maria

doi:10.1016/s0304-3940(00)01533-0

Cited by 34 publications

(22 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this paper, we have established the localisation of the expression of NGF protein and the gene in the neonate mouse uterus and show it to be exclusively located in uterine luminal epithelial cells. The role of NGF in the uterus is unclear although it has been suggested that NGF is an important developmental regulator in the uterus and implicated in uterine reinnervation after pregnancy (Brauer et al 2000, Varol et al 2000. There is increasing evidence that NGF is under hormonal control in various tissues (Jehan et al 1993, Veenstra et al 1998, Pan et al 1999) and we further demonstrate this with oestradiol in the mouse uterus.…”

Section: Discussionsupporting

confidence: 60%

See 1 more Smart Citation

Comparison of the effect of oestradiol, tamoxifen and raloxifene on nerve growth factor-alpha expression in specific neonatal mouse uterine cell types using laser capture microdissection

Green

Edwards²,

Greaves³

et al. 2003

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

Oral dosing of CD-1 mice on days 2-5 after birth with tamoxifen but not raloxifene disrupts the development of the myometrium, resulting in adult uterine adenomyosis. Using laser capture microdissection and RT-PCR we have investigated nerve growth factor (NGF) and cognate receptor expression in uterine cells of 6-day-old pups that may be important in early developmental changes that give rise to adenomyosis. NGF down-regulation is known to occur during terminal myogenic differentiation.NGF was found exclusively in endometrial luminal epithelium of controls. It was up-regulated 18-fold in the luminal epithelium following dosing with tamoxifen but not raloxifene. Western blotting for NGF protein in the whole uterus showed a 25-fold increase after tamoxifen treatment. Expression of the low affinity p75 neutrophin receptor (p75 NTR ) was twofold higher in the myometrium compared with luminal epithelium or stroma. This was not altered following tamoxifen treatment. There was no detectable expression of high affinity tyrosine kinase receptor (trkA NGFR ). This study shows luminal epithelial cells of the endometrium primarily form NGF. This suggests that NGF normally regulates the differentiation of the mesenchyme into uterine myocytes through paracrine mechanisms and that an early disturbance of this process plays a key role in the subsequent development of adenomyosis.

show abstract

Section: Discussionsupporting

confidence: 60%

“…The expression of NGF in the uterus has previously been described (Varol et al 2000. In this paper, we have established the localisation of the expression of NGF protein and the gene in the neonate mouse uterus and show it to be exclusively located in uterine luminal epithelial cells.…”

Section: Discussionmentioning

confidence: 61%

Comparison of the effect of oestradiol, tamoxifen and raloxifene on nerve growth factor-alpha expression in specific neonatal mouse uterine cell types using laser capture microdissection

Green

Edwards²,

Greaves³

et al. 2003

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

show abstract

“…This possibility is supported by our recently reported intraocular transplantation studies showing that both estrogen (Brauer et al 2000a) and pregnancy (Brauer et al 1998) affect the receptivity of the myometrial tissue to sympathetic nerve fibers. Although the nature of the signals produced by the target has not yet been elucidated, it is possible that sex hormones affect the pattern of growth of uterine projecting neurons via changes in the production of target-derived neurotrophic factors (Thoenen 1995;Cowen and Gavazzi 1998;Gallo and Letourneau 1998;Naves et al 1998;Baloh et al 2000;Brauer et al 2000b,c;Varol et al 2000), changes in signals provided by the extracellular matrix (de Curtis 1991; Gavazzi et al 1995;Tessier-Lavigne and Goodman 1996), or changes in the receptivity of neurons to the signals produced by the target (Toran-Alleran 1996).…”

Section: Discussionmentioning

confidence: 99%

Effects of Infantile/Prepubertal Chronic Estrogen Treatment and Chemical Sympathectomy with Guanethidine on Developing Cholinergic Nerves of the Rat Uterus

Richeri

Viettro

Chávez-Genaro

et al. 2002

J Histochem Cytochem.

View full text Add to dashboard Cite

(TC) S U M M A R Y The innervation of the uterus is remarkable in that it exhibits physiological changes in response to altered levels in the circulating levels of sex hormones. Previous studies by our group showed that chronic administration of estrogen to rats during the infantile/prepubertal period provoked, at 28 days of age, an almost complete loss of norepinephrine-labeled sympathetic nerves, similar to that observed in late pregnancy. It is not known, however, whether early exposure to estrogen affects uterine cholinergic nerves. Similarly, it is not known to what extent development and estrogen-induced responses in the uterine cholinergic innervation are affected by the absence of sympathetic nerves. To address this question, in this study we analyzed the effects of infantile/prepubertal chronic estrogen treatment, chronic chemical sympathectomy with guanethidine, and combined sympathectomy and chronic estrogen treatment on developing cholinergic nerves of the rat uterus. Cholinergic nerves were visualized using a combination of acetylcholinesterase histochemistry and the immunohistochemical demonstration of the vesicular acetylcholine transporter (VAChT). After chronic estrogen treatment, a well-developed plexus of cholinergic nerves was observed in the uterus. Quantitative studies showed that chronic exposure to estrogen induced contrasting responses in uterine cholinergic nerves, increasing the density of large and medium-sized nerve bundles and reducing the intercept density of fine fibers providing myometrial and perivascular innervation. Estrogen-induced changes in the uterine cholinergic innervation did not appear to result from the absence/impairment of sympathetic nerves, because sympathectomy did not mimic the effects produced by estrogen. Estrogen-induced responses in parasympathetic nerves are discussed, considering the direct effects of estrogen on neurons and on changes in neuron-target interactions.

show abstract

“…Although the nature of the signals produced by the sex-hormoneprimed uterus is still unknown (Brauer et al 2000b;Varol et al 2000), it is possible that oestrogen could affect the neurotrophic capacity of the uterus. Because sympathetic nerves are susceptible to changes in the availability of NGF, we have assessed the possibility that oestrogen can reduce the levels of NGF in the rat uterus.…”

Section: Effects Of Chronic Oestrogen On the Reinnervation Of Intraocmentioning

confidence: 99%

Differential effects of oestrogen on developing and mature uterine sympathetic nerves

Chávez-Genaro

Crutcher

Viettro

et al. 2002

Cell and Tissue Research

View full text Add to dashboard Cite

Oestrogen is a key factor in the remodelling of uterine sympathetic nerves during puberty and the oestrous cycle; these nerves are influenced by changes in their target uterine tissue. The magnitude of oestrogen-induced responses might however be influenced by the maturation stage of sympathetic nerve fibres, the age of the neurons and/or the developmental state of the uterus. We have therefore compared the sympathetic innervation of the uterus following chronic oestrogen treatment of infantile/prepubertal and young adult intact and ovariectomised rats. Treatment of infantile/prepubertal rats resulted in the complete loss of intrauterine noradrenaline (NA)-labelled sympathetic nerves and a marked reduction in the total NA content in the uterine horn. Chronic treatment of young adult rats had little effect. To examine whether the age of the neurons or the degree of development of the uterus determined responsiveness of nerves to oestrogen, we assessed the effects of oestrogen on the sympathetic reinnervation of intraocular transplants of young adult uterine myometrium into ovariectomised adult host rats. Early treatment (10 days post-transplantation) resulted in less sympathetic innervation than late treatment (30 days post-transplantation). Measurements of nerve growth factor (NGF) levels in the uterine horn of control rats before and after puberty and following infantile/prepubertal chronic oestrogen treatment and acute oestrogen treatment of young adult rats revealed a coordinated increase between the growth of the uterus and NGF protein levels. Thus, developing and recently regrown sympathetic nerves are more susceptible to oestrogen-induced changes in the uterus than mature nerves, differential susceptibility is not related to the age of the neurons or the developmental state of the uterus and changes in NGF protein do not account for the differential susceptibility of developing and mature uterine sympathetic nerve fibres to oestrogen. Growing sympathetic fibres are more vulnerable to oestrogen than mature fibres and nerve fibres that have been in contact for longer periods with their target become less susceptible to oestrogen.

show abstract

Nerve growth factor (NGF) and NGF mRNA change in rat uterus during pregnancy

Cited by 34 publications

References 18 publications

Comparison of the effect of oestradiol, tamoxifen and raloxifene on nerve growth factor-alpha expression in specific neonatal mouse uterine cell types using laser capture microdissection

Comparison of the effect of oestradiol, tamoxifen and raloxifene on nerve growth factor-alpha expression in specific neonatal mouse uterine cell types using laser capture microdissection

Effects of Infantile/Prepubertal Chronic Estrogen Treatment and Chemical Sympathectomy with Guanethidine on Developing Cholinergic Nerves of the Rat Uterus

Differential effects of oestrogen on developing and mature uterine sympathetic nerves

Contact Info

Product

Resources

About