Estrogen Regulation of c-<i>fos</i>Messenger Ribonucleic Acid

Loose-Mitchell, David S.; Chiappetta, Constance; Stancel, George M.

doi:10.1210/mend-2-10-946

Cited by 199 publications

(84 citation statements)

References 33 publications

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“…Such a finding is congruent with the earlier observation that estrogens stimulate growth of the pituitary through replication of the prolactin-secreting cells in F344 rats but not in outbred rat strains (11-13). We also found that the uterine epithelium of F344 rats but not that of S-D rats exhibited a hypertrophic response to BPA administered in low doses (2 (15)(16)(17)(18). The induction of these genes is believed to play a key role in cell proliferation (19,20).…”

mentioning

confidence: 61%

Strain differences in vaginal responses to the xenoestrogen bisphenol A.

Long

Steinmetz

Ben‐Jonathan

et al. 2000

Environ Health Perspect

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Bisphenol A (BPA) is the monomer component of polycarbonate plastics and epoxy resins; human exposure derives from leachate in foodstuffs packaged in certain plastics or from epoxybased dental appliances. BPA (6). Although it is almost entirely in its polymerized form, the BPA monomer finds its way into foodstuffs as a leachate of plastic packaging (7,8). Also, humans can be exposed to BPA from certain dental appliances (9,10). Because of its estrogenic activity, there is concern over human exposure to BPA.When assessing the biologic activity of a putative estrogenic compound in animal model systems, it is important to consider species and strain differences. We previously found that BPA increased blood prolactin levels in Fischer 344 (F344) but not SpragueDawley (S-D) rats (3). Such a finding is congruent with the earlier observation that estrogens stimulate growth of the pituitary through replication of the prolactin-secreting cells in F344 rats but not in outbred rat strains (11-13). We also found that the uterine epithelium of F344 rats but not that of S-D rats exhibited a hypertrophic response to BPA administered in low doses (2 (15)(16)(17)(18). The induction of these genes is believed to play a key role in cell proliferation (19,20). In the present study, we determined the potency of BPA to induce immediate early gene expression and DNA synthetic activity in the vaginal epithelium of F344 and S-D rats. Materials and MethodsAnimals. All procedures performed on animals followed the NIH Guide for the Care and Use ofLaboratory Animals (21) and were approved by the Indiana University Animal Care and Use Committee. F344 and S-D rats were supplied at 6-8 weeks of age by Harlan Sprague-Dawley (Indianapolis, IN). One week after arrival, animals were ovariectomized under ketamine anesthesia; they were subjected to experimental manipulation 3 weeks later. BPA (Aldrich Chemical Co., Milwaukee, WI) and 17,B-estradiol (E2; Sigma Chemical Company, St. Louis, MO) were dissolved in ethanol and diluted in sesame oil. Compounds were injected intraperitoneally (ip) in 50 pL of solution. We injected BPA at 0.2-150 mg/kg body weight (bw) and E2 at 0.02-2.0 pg/kg bw.Bromodeoxyuridine immunostaining. Animals were injected with bromodeoxyuridine (BrdU; 100 mg/kg bw in 500 pL saline, ip) and killed 1 hr later. Tissue taken from treated animals was fixed in ethanol-chloroform-acetic acid (60:30:10, vol/vol/vol)

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mentioning

confidence: 61%

Strain differences in vaginal responses to the xenoestrogen bisphenol A.

Long

Steinmetz

Ben‐Jonathan

et al. 2000

Environ Health Perspect

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“…Our results, however, indicate that both DES and Tx act as ER inducer in the uterus and vagina in both neonatal and ovariectomized adult mice, although ER mRNA induction time of Tx is slower than that of DES in neonatal mice. Estrogens including DES evoke the early response of genes, jun and fos proto-oncogenes, whose products control the cell cycle (Loose-Mitchell et al, 1988;Weisz and Bresciani, 1988;Kamiya et al, 1995). Tamoxifen also raises the uterine activity levels of these protooncogenes in rats (Kirkland et al, 1993;Nephew et al, 1993) and in mice (Nishimura et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Estrogen receptor (ER) and its messenger ribonucleic acid expression in the genital tract of female mice exposed neonatally to tamoxifen and diethylstilbestrol

et al. 1996

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“…Estrogen-mediated hyperpolarization of PAG-RVM neurons would provide a direct mechanism whereby morphine failed to elicit Fos in PAG-RVM neurons. Alternatively, as the gene encoding Fos contains an estrogen response element (Loose-Mitchell et al, 1988,Wang et al, 2003, changes in cycle status may have potentially influenced the ability of morphine to induce Fos in PAG-RVM neurons in females. Lastly, estradiol has also been shown to induce MOR internalization (Eckersell et al, 1998,Sinchak and Micevych, 2001,Micevych et al, 2003,Mills et al, 2004; this would limit the amount of receptor available for ligand binding and would thereby potentially decrease morphine's ability to induce Fos in PAG-RVM neurons.…”

Section: The Pag-rvm Circuit Is Preferentially Activated In Male Ratsmentioning

confidence: 99%

Morphine preferentially activates the periaqueductal gray–rostral ventromedial medullary pathway in the male rat: A potential mechanism for sex differences in antinociception

2007

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The midbrain periaqueductal gray (PAG), and its descending projections to the rostral ventromedial medulla (RVM), provides an essential neural circuit for opioid-produced antinociception. Recent anatomical studies have reported that the projections from the PAG to the RVM are sexually dimorphic and that systemic administration of morphine significantly suppresses pain-induced activation of the PAG in male but not female rats. Given that morphine antinociception is produced in part by disinhibition of PAG output neurons, it is hypothesized that a differential activation of PAG output neurons mediates the sexually dimorphic actions of morphine. The present study examined systemic morphine-induced activation of PAG-RVM neurons in the absence of pain. The retrograde tracer fluorogold (FG) was injected into the RVM to label PAG-RVM output neurons. Activation of PAG neurons was determined by quantifying the number of Fos-positive neurons one hour following systemic morphine administration (4.5 mg/kg). Morphine produced comparable activation of the PAG in both male and female rats, with no significant differences in either the quantitative or qualitative distribution of Fos. While microinjection of FG into the RVM labeled significantly more PAG output neurons in female rats than male rats, very few of these neurons (20%) were activated by systemic morphine administration in comparison to males (50%). The absolute number of PAG-RVM neurons activated by morphine was also greater in males. These data demonstrate widespread disinhibition of PAG neurons following morphine administration. The greater morphine-induced activation of PAG output neurons in male compared to female rats is consistent with the greater morphine-induced antinociception observed in males. Keywordspain; morphine analgesia; pain inhibition; opioid; sexual dimorphism endogenous descending pathway Morphine and other mu-opioid receptor agonists are the most effective pharmacological treatment for the alleviation of persistent pain. However, it is becoming increasingly clear that morphine does not produce the same degree of analgesia in males and females. In the majority of studies reported to date, morphine produced a greater antinociceptive response in males in Correspondence to: Anne Z. Murphy, Ph.D., Dept. Biology, Center for Behavioral Neuroscience, Georgia State University, PO Box 4010, Atlanta, amurphy@gsu.edu, Phone: 404.463.9661, Fax: 404.651.2509 Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. (Bodnar et al., 1988,Craft, 2003b,Craft, 2003a,Cook and Nickerson, 2005,Wang et al., 2006. Sex difference...

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Estrogen Regulation of c-fosMessenger Ribonucleic Acid

Cited by 199 publications

References 33 publications

Strain differences in vaginal responses to the xenoestrogen bisphenol A.

Strain differences in vaginal responses to the xenoestrogen bisphenol A.

Estrogen receptor (ER) and its messenger ribonucleic acid expression in the genital tract of female mice exposed neonatally to tamoxifen and diethylstilbestrol

Morphine preferentially activates the periaqueductal gray–rostral ventromedial medullary pathway in the male rat: A potential mechanism for sex differences in antinociception

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