• The korean journal of orthodontics
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• v.30 no.4 s.81
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• pp.441-452
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• 2000

The present studies were performed to investigate the interaction of $17{\beta}$-estradiol and human growth hormone(hGH) on the proliferation of human periodontal ligament(WDL) cell. The independent effects of $17{\beta}$ estradiol and hGH on hPDL cell proliferation were investigated and the effects of hGH on hPDL cell proliferation after $17{\beta}$-estradiol pre-treatment were also investigated. Lastly, the change of hGH receptor expression in hPDL cell after $17{\beta}$-estradiol pre-treatment were investigated. The obtained results were as follows; 1. The treatment of $17{\beta}$-estradiol or hGH had no significant effects on hPDL cell proliferation. 2. After pre-treatment of $17{\beta}$-estradiol, hGH stimulated the proliferation of the hPDL cell, regardless of hHG concentration. 3. Although there was not hGH receptor in the hPDL cell, hGH receptors were expressed in hPDL cell after more than 6 hours pre-treatment of $17{\beta}$-estradiol. 4. The effect of hGH on hPDL cell proliferation was related to the hGH receptor expression. $17{\beta}$-estradiol pre-treaaent contributed to the hGH effects on the hPDL cell by stimulating hGHR expression.

• Korean Journal of Veterinary Service
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• v.31 no.4
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• pp.457-463
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• 2008

The sex steroid hormone estradiol-$17{\beta}(E_2)$ mediate their biological effects on development, differentiation and maintenance of reproductive tract and other target tissue through gene regulation by nuclear steroid receptors. Although the importance of $E_2$ in many physiological process has been reported, but little is known about the effects of $E_2$ on primary cultured chicken hepatocyte. therefore, in the present study, we have examined the effect of $E_2$ on cell proliferation and it's related signal cascades. $E_2$ increase $[^3H]$-thymidine incorporation in time-(${\leq}8hr$) and dose-($10^{-10}M$)dependent manner and treatment of $E_2$ increased the phosphorylation of p44/43 MAPKs(p44/42 mitogen-activated protein kinase) and JNK(c-Jun N-terminal kinase) in a time dependent manner. In addition, PD98059(p44/42 blocker, $10^{-5}M$), SP600125(JNK blocker, $10^{-6}M$) blocked the estrogen-induced increase in $[^3H]$-thymidine incorporation. In conclusion, $E_2$ stimulates the proliferation of primary cultured chicken hepatocytes and this action is mediated by p44/42 MAPKs and JNK signal transduction pathway.

• Journal of Gastric Cancer
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• v.13 no.3
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• pp.172-178
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• 2013

Purpose: The aims of this study were as follow: 1) to de scribe the expression status of estrogen receptor-${\alpha}$ and -${\beta}$ mRNAs in five gastric carcinoma cell lines; 2) to evaluate in vitro the effects of $17{\beta}$-estradiol and estrogen receptor antagonists on the proliferation of the cell lines. Materials and Methods: Detection of estrogen receptor-${\alpha}$ and estrogen receptor-${\beta}$ mRNA in five human gastric cancer cell lines (AGS, KATO III, MKN28, MKN45 and MKN74) was made by the reverse transcription-polymerase chain reaction system. To evaluate the effect of $17{\beta}$-estradiol and estrogen receptor antagonists on the proliferation of gastric cancer cell line, the cell lines which expressed both es trogen receptors were chosen and treated with $17{\beta}$-estradiol and estrogen receptor antagonists (methyl-piperidino-pyrazole and pyrazolo [1,5-a] pyrimidine). Cell proliferation was assessed with the methylthiazol tetrazolium test. Results: Estrogen receptor-${\alpha}$ and estrogen receptor-${\beta}$ mRNAs were expressed in three (KATO III, MKN28 and MKN45) and all of the five gastric cancer cell lines, respectively. At higher concentrations, $17{\beta}$-estradiol inhibited cell growth of MKN28, MKN45 and KATO III cell lines. Neither estrogen receptor-${\alpha}$ nor estrogen receptor-${\beta}$ antagonist blocked the anti-proliferative effect of $17{\beta}$-estradiol. Conclusions: Our results indicate that estrogen receptor-${\beta}$ mRNAs are preferentially expressed in gastric cancers and also imply that hormone therapy rather than estrogen receptor blockers may be a useful strategy for the treatment of estrogen receptor-${\beta}$ positive gastric cancer. Its therapeutic significance in gastric cancer are, however, limited until more evidence of the roles of estrogen receptors in the gastric cancer are accumulated.

• Korean Journal of Veterinary Research
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• v.37 no.2
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• pp.311-319
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• 1997

The mechanisms of $estradiol-17{\beta}$ regulating growth of both normal and neoplastic cells are not clear until now. In studies using various estrogen-dependent breast cell lines, it is recently known that estrogen controls the cell growth by regulating the expression of growth factors and/or their receptors. In the present study, we investigated the effects of $estradiol-17{\beta}$on cell growth and IGF-I binding sites using primary cultured renal proximal tubule cells. We have obtained results as follows : $Estradiol-17{\beta}(10^{-9})$ has stimulatory effects in cell growth. Cotreatment of $estradiol-17{\beta}(10^{-9}M)$ and $IGF-I(5{\times}10^{-8}M)$ significantly increased the growth of primary rabbit renal proximal tubule cells compared to that of $estradiol-17{\beta}$ or IGF-I alone treated cells. In binding studies, we found that the binding of $^{125}IGF-I$ on cell membranes was incubation time- and temperature-dependent. Incubation at $37^{\circ}C$ results in higher binding of $^{125}IGF-I$ than that of $23^{\circ}C$ or $4^{\circ}C$. Maximum binding was observed at $37^{\circ}C$ between 30 and 60 minutes. The binding of $^{125}IGF-I$ to both control and $estradiol-17{\beta}-treated$ cells was inhibited by unlabelled $IGF-I(10^{-8}{\sim}10^{-12}M)$ in a concentration-dependent manner. However, EGF did not compete for $^{125}IGF-I$ binding at $10^{-8}{\sim}10^{-12}M$. IGF-I binding to the membranes from both control and $estradiol-17{\beta}-treated$ cells was also analyzed. We found that $estradiol-17{\beta}-treated$ cells exhibited higher binding activity for IGF-I. When $estradiol-17{\beta}$ or tamoxifen alone, or $estradiol-17{\beta}$ and tamoxifen cotreated cells were compared, the binding ratio of $^{125}I-IGF-I$ of $estradiol-17{\beta}-treated$ cell was significantly increased but was similar to control in both $estradiol-17{\beta}$ and tamoxifen cotreated cell. These results suggest that $estradiol-17{\beta}$ in part controls cell proliferation by regulating the expression of IGF-I receptors in primary rabbit renal proximal tubule cells.

• Asian-Australasian Journal of Animal Sciences
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• v.13 no.2
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• pp.161-166
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• 2000

This study was designed to determine the effects of the insulin-like growth factor (IGF-1) and estradiol $17-{\beta}$ on the in vitro proliferation of stromal vascular cell from Hanwoo omental, subcutaneous, intermuscular and intramuscular adipose tissues. Cells were cultured in M199+20% newborn calf serum and the proliferation of cells was measured by direct microscopic cell counting and change of genomic DNA amount. Cell numbers increased slightly over the first 72 hour of culture and then increased greatly, regardless of adipose tissue depots. In IGF-1 treatment, the number of omental preadipocytes maintained highest level from the beginning to the 20th day of culture. However, in estradiol-$17{\beta}$ treatment, those tended to be lower than the control from the beginning of culture and significantly lower at the 24th day. When IGF-1 was added to subcutaneous preadipocytes, the numbers of cells were higher from 11th day than those from other treatments, although there was no statistical significance. For intermuscular preadipocytes treated with IGF-1, its numbers were significantly (p<0.05) higher at 11th day, and in the other days it showed a similar tendency to those of the subcutaneous tissue. In this experiment, preadipocytes were taken from 24 month old fully matured steers and the highest proliferation rate was shown in intramuscular tissue followed by those of subcutaneous preadipocytes. Addition of $5{\mu}M$ estradiol-$17{\beta}$ to the growth medium failed to promote the replication of Hanwoo preadipocytes, as indicated by direct cell counts and total genomic DNA content. As the culture period proceeded, the amounts of DNA were increased, but the patterns of increment were not consistent with the results of cell numbers.

• Journal of Periodontal and Implant Science
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• v.30 no.2
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• pp.375-390
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• 2000

The purpose of this study is to evaluate the expression ofIGF-I, considered as the mediator of action of estrogen, and IGF-IA and IGF-IB, alternative slicing form of IGF-I, using $17{\beta}-estradiol$ in MC3T3-E1 cells. We observed the effect on type I collagen and osteopontin gene expression and DNA synthetic activity of MC3T3-E1 cells, added by estrogen, IGF-I and combination and the interactionon proliferation and differentiation of MC3T3-E1 cells. The results were as follows :RT-PCR experiment for observing timedependantIGF-I gene expression patternshowed IGF-IA and IB gene expression in both of control and test group. In these IGF-IA gene expression was appeared predominantly. In control, IGF-I geneexpression level was maintained until 24hr and then decreased gradually. In testgroup, IGF-I gene expression level increased as time goes by. Experiment measuring DNA synthetic activity, as it is added by $17{\beta}-estradiol$, IGF-I and combination, showed that first day , there was the tendency of more increase of synthetic activity in all test group than control but no statical significance(P>0.05), and third day, there was more increase of DNA synthetic activity in $17{\beta}-estradiol$ group and combination group and it was statically significant. (P<0.005) Experiment for observing type I collagen gene expression pattern showed more increase of expression in $17{\beta}-estradiol$ group than control and no significant difference in IGF-I group and combination group. Experiment for observing osteopontin gene expression pattern showed no significant difference in control and test group. In conclusion, $17{\beta}-estradiol$ in MC3T3- E1 cells increased IGF-I gene and DNA synthetic activity simultaneously, therefore it appeared that IGF-I is related to the action of estrogen. Combination treatment of IGF-I and $17{\beta}-estradiol$ has effect on cell proliferation but this effect is lower than IGF-I or $17{\beta}-estradiol$ alone. However, combination treatment has not great effect on type I collagen or osteopontin gene expression thus little effect of cell differentiation.

• Journal of Animal Science and Technology
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• v.52 no.3
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• pp.175-186
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• 2010

The aim of this study was to analyze the proteome expressions of proliferating stromal vascular cells from Hanwoo omental, subcutaneous and intramuscular depots subjected to hormone deprivation and IGF-1, Estradiol-$17{\beta}$ addition. For hormone deprivation or addition studies, the cells were either grown in 10% charcoal-dextran stripped fetal bovine serum (CD-FBS) or in 10% FBS supplemented medium. Further, to analyze the effect of insulin like growth factor (IGF-1) and $17\beta$-Estradiol (E2), cells were grown in 10% CD-FBS containing IGF-1 (10 ng/ml) or E2 (10 nM). The results showed that hormone deprivation had a negative impact on proliferation among the cells from all depots without any growth difference. On comparison of proliferation levels, higher levels were observed in cells that were grown in 10% FBS than in 10% CD-FBS alone or with IGF-1/E2. Proteome expression from preadipocytes grown in hormone deprivation conditions were compared by 2D-DIGE and MALDIToF/ToF. A total of twelve different proteins were found to be differentially expressed under hormone deprivation conditions. Further, our proteomic analysis with DIGE under IGF-1 and E2 addition revealed four proteins with differential expression levels. Moreover, the results highlighted in this study offer a role for each differentially expressed protein with respect to their effect in positive or negative regulation on proliferation.

• Journal of Food Hygiene and Safety
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• v.22 no.3
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• pp.209-212
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• 2007

To evaluate the estrogenic activities of di-ethyl hexyl phthalate (DEHP) and di-butyl phthalate (DBP), two phthalates known as endocrine disrupters, we used MCF-7 human breast cancer cell line. As results, DBP and DEHP had estrogenic effects. In brief, the concentration of maximal MCF-7 cell proliferation was $10^{-7}M\;and\;10^{-8}M$ for DEHP and DBP, respectively. The ratio of maximal cell yield of the test compounds to that of $17{\beta}-estradiol$ was 87.5% for DEHP and 73.4% for DBP. In summary, both DEHP and DBP had cell proliferation potencies in the MCF-7 cell. Potencies ranged from approximately 10 to 100 times less than 17beta-estradiol. DBP was stronger than DEHP in the concentration of maximal efficacy. However, DEHP was stronger than DBP in the MCF-7 cell proliferation. Results from this study suggested that DEHP and DBP may play an important role in the estrogenic activity. Therefore, it is suggested that DEHP and DBP are estrogenic.

• Journal of Life Science
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• v.24 no.2
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• pp.173-180
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• 2014

Estrogen can promote or inhibit cellular proliferation depending on tissue cell types and physiological condition and acts through the signal transduction pathways mediated primarily by estrogen receptors. This study examined the effects of fulvestrant (Ful), a well-known antagonist for the estrogen receptor, on the action of $17{\beta}$-estradiol (E2) with respect to the proliferation and apoptosis of Chinese hamster ovarian (CHO) cells. We used different concentrations of E2, Ful, and E2 plus Ful during different treatment durations. Treatment with 15-40 ${\mu}M$ E2 significantly inhibited proliferation in a time-dependent manner, although it had no influence in concentrations up to 1 ${\mu}M$. Interestingly, Ful at 10-40 ${\mu}M$ also inhibited cellular proliferation in both a concentration- and time-dependent manner. In addition, Ful enhanced rather than decreased the inhibitory effect on cellular proliferation by E2 in combined treatment for 10 days. Thus, Ful does not appear to have an antagonistic effect on estrogen's anti-proliferative action in CHO cells. In TUNEL assays to confirm DNA fragmentation by E2 and/or Ful, CHO cells treated with 20 ${\mu}M$ E2 showed a TUNEL-positive reaction in most DAPI-stained nuclei, and cells treated with either 40 ${\mu}M$ Ful or 40 ${\mu}M$ Ful plus 20 ${\mu}M$ E2 also exhibited a TUNEL-positive reaction but at a lower rate compared to the E2-treated cells. These results indicate that Ful does not have an antagonistic effect on estrogen's anti-proliferative action in CHO cells, suggesting that the anti-proliferative and apoptosis-related mechanism(s) through DNA fragmentation by E2 and Ful may be mediated by different signal transduction pathways.

• The Journal of Korean Medicine
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• v.29 no.2
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• pp.71-80
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• 2008

Objective: There is increasing evidence that chronic non-bacterial prostatitis is recognized to be a local inflammatory disease, and there is substantiating evidence to support the role of the inflammatory responses in its pathogenesis, and clinical value in the evaluation of therapeutic efficacy. Prunella vulgaris has been traditionally used in treatment of inflammatory diseases, including of scrofula, goiter, and allergy diseases. In this study, we investigated the effects of Prunella vulgaris on inflammatory cytokines and cytopathological alternation in the rat model of non-bacterial prostatitis induced by castration and $17{\beta}-estradiol$ treatment. Methods: Two-month-old rats were treated with $17{\beta}-estradiol$ after castration for induction of experimental non-bacterial prostatitis, which is similar to human chronic prostatitis in histopathological profiles. Prunella vulgaris as an experimental specimen, and testosterone as a positive control, were administered orally. The prostates were evaluated by histopathological parameters including the epithelial score and epithelial-stromal ratio for glandular damage, and the expression of inflammatory cytokine genes including the interleukin $(IL)-1{\beta}$, IL-5, IL-12, and tumor necrosis factor $(TNF)-{\alpha}$. Results: While prostates of control rats revealed severe acinar gland atrophy and stromal proliferation, the rats treated with Prunella vulgaris showed a diminished range of tissue damage. Epithelial score was improved in Prunella vulgaris over that of the control (P<0.05). The epithelial-stromal ratio was lower with Prunella vulgaris when compared to that of the control (P<0.05). In the reverse transcription-polymerase chain reaction (RT-PCR) of inflammatory cytokine genes, Prunella vulgaris inhibited the expression of $IL-1{\beta}$ and $TNF-{\alpha}$ genes, while it modulated the expression of IL-5, which is an anti-inflammatory cytokine. Conclusions: These findings suggest that Prunella vulgaris may protect the glandular epithelial cells and also inhibit stromal proliferation in association with the immune modulation including the suppression of inflammatory cytokines and promotion of anti-inflammatory cytokine. From theses results, we suggest that Prunella vulgaris could be a useful remedy agent for treating chronic non-bacterial prostatitis.