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ABSTRACT: Context: Müllerian inhibiting substance (MIS) is produced in Sertoli cells of fetal testis and causes regression of Müllerian ducts in male embryos. MIS also can induce the cell cycle arrest and apoptosis in Müllerian duct-derived tumors in vivo and in vitro. Objective: Our objective was to investigate the expression of MIS type II receptor (MISR II) and whether MIS can inhibit the proliferation and induce apoptosis in primary cultures of endometrial stromal cells (ESC) of endometriosis. Design and Settings: In vitro experiments were performed in the university research laboratory. Participants: Tissue samples from 12 patients who had undergone evisceration for ovarian endometrial cysts were included in this study. Interventions and Main Outcome Measures: The expression of MISR II in ESC was investigated by immunohistochemistry. The cell viability and apoptosis in ESC treated with MIS was measured by methylthiazoletetrazolium assay and annexin V analysis. The expression of regulatory proteins in ESC treated with MIS was shown by Western blotting. Results: ESC showed specific immunostaining for the MISR II. ESC treated with MIS exhibited 32% growth inhibition (P = 0.0001). The changes in cell cycle distribution after MIS exposure at 72 h demonstrated that S and G(2)M phases were decreased; G(0)G(1) and sub-G(0)G(1) phases were increased. ESC treated with MIS showed 13.72% annexin V-fluorescein isothiocyanate positivity. In the ESCs, which contain defective p16, MIS increased the expression of pocket proteins p107 and p130 and decreased E2F transcription factor 1. Conclusions: The results support a central role for MIS in endometriosis. Although the precise mechanism of MIS-mediated inhibition of ESC growth has not been fully defined, these data suggest that MIS has activity against ESC in vitro and may also be an effective targeted therapy for endometriosis.
The Journal of clinical endocrinology and metabolism 07/2012; 97(9):3224-30. · 6.50 Impact Factor
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ABSTRACT: This study aimed to analyze expression of Müllerian inhibiting substance type II receptor (MISRII) protein and mRNA in cervical neoplasia, to demonstrate the growth inhibition of cervical cancer cells by administration of highly purified recombinant human Müllerian inhibiting substance (MIS) and, furthermore, to evaluate the clinical significance of MIS as a biological modifier for MIS receptor expressing tumors. Reverse transcriptase polymerase chain reaction (RT-PCR) was used for MISRII mRNA expression, and in situ hybridization and immunohistochemistry were used to observe expression, location of MISRII mRNA and protein, respectively. To demonstrate the effect of MIS on the viability of cervical cancer cells, methyl thiazole tetrazolium (MTT) assay was performed. Flow cytometry was used to evaluate the cell cycle distribution after exposure to MIS in cervical cancer cells, and the annexin-V-FITC staining method was performed to demonstrate apoptosis by MIS in cervical cancer cells. Expression of MISRII protein and mRNA were observed in all normal cervical and cervical carcinoma tissues. There was no significant difference in expression of MISRII protein and MISRII mRNA between normal cervical and cervical carcinoma tissues. MTT assay showed negative correlation between MIS exposure time and the viability of cervical cells (P=0.008). The changes in cell cycle distribution after MIS exposure suggest that MIS plays an important role in inducing cellular apoptosis by causing arrest at the G1 phase and increasing cells at sub-G0G1 phase. Annexin-V-FITC staining methods showed that cellular apoptosis was, respectively, 10.44 and 12.89% after 24 and 48 h of MIS exposure in cervical carcinoma cells. There was a negative correlation between cellular survival and MIS exposure time. This study demonstrates that MISRII is present on normal cervical and cervical carcinoma tissues, and MIS shows receptor-mediated antiproliferative effect on cervical cells in vitro. These data suggest that MIS may be used as a biological modifier or therapeutic modulator on MISRII-expressing tumors in the future.
International Journal of Oncology 02/2012; 40(6):2013-21. · 2.40 Impact Factor
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Jae-Yen Song,
Seong-Jin Hwang,
Min-Joung Kim,
Hyun-Hee Jo,
Sue-Yeon Kim,
Kwang-Eun Choi,
Dong-Jin Kwon,
Young-Ok Lew,
Jang-Heub Kim,
Yong-Taik Lim,
Jin-Hong Kim,
Eun-Jung Kim,
Mee-Ran Kim
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ABSTRACT: In this article, we would like to compare the clinical characteristics and effectiveness of selective uterine artery double ligation and bipolar uterine artery coagulation in total laparoscopic hysterectomy (TLH) retrospectively. TLH was performed on 72 patients with selective uterine artery double ligation and on 312 patients with uterine artery bipolar coagulation in tertiary university hospital from January 2004 through January 2006. Both groups were similar with respect to age, body mass index, parities, rate of menopause and uterine weight. The mean transfusion, postoperative hospital stay and drain insertion in the selective uterine artery double ligation group were significantly lower than those in the bipolar uterine artery coagulation group in TLH, respectively (p < .05). There were no differences in the hemoglobin, hematocrite change, additional operations, operation time, rate of complication between the two kinds of operation (p > .05). In conclusion, selective uterine artery double ligation in TLH showed lower transfusion rate, less hospitalization and less discomfort due to drain than bipolar uterine artery coagulation. Also, it did not take a longer time for operation and thus provides a feasible and secure method to manage uterine vessels at the level of uterine isthmus inside of the broad ligament.
Minimally invasive therapy & allied technologies: MITAT: official journal of the Society for Minimally Invasive Therapy 08/2010; 19(4):224-30. · 1.33 Impact Factor
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Jae-Yen Song,
Min-Joung Kim,
Hyun-Hee Jo,
Seong-Jin Hwang,
Boah Chae,
Jae-Eun Chung,
Dong-Jin Kwon,
Young-Ok Lew,
Yong-Taik Lim,
Jang-Heub Kim,
Jin-Hong Kim,
Mee-Ran Kim
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ABSTRACT: This study discussed the role of estrogen as an antioxidant in the damage of vascular endothelial cells.
We treated bovine aortic endothelial cells (bAEC) either with 1mM of H(2)O(2) alone or with 1 microM of 17beta-estradiol (E(2)) for 24h followed by 1mM of H(2)O(2) for 3h. The cell survival was evaluated by MTT assay, cellular apoptosis by fluorescence activated cell sorter (FACS) and Hoechst 33342 staining, oxidative stress by intracellular reactive oxygen species (ROS) and apoptosis after oxidative stress by western blotting for phospho-p38, p38, and Bcl-2.
MTT assay showed that bAEC viability was reduced to 55.7+/-3.0% and 39.1+/-3.7% after 30 and 60 min of H(2)O(2) treatment, respectively. E(2) and H(2)O(2) treated cells did not show significant decrease in the cell survival. Similarly the FACS analysis and Hoechst 33342 stain showed that the latter decreased cellular apoptosis induced by H(2)O(2). Intracellular ROS increased by 181.6+/-68.9% in the former and by 37.0+/-3.9% in the latter (P<0.05). The expression of phospho-p38 mitogen-activated protein kinase (MAPK) was higher in the latter.
E(2) mediates antioxidant effects on the oxidative stress induced by H(2)O(2). This antioxidant effect on bAEC may elucidate the scientific basis of hormone therapy for maintaining cardiovascular integrity in postmenopausal women.
The Journal of steroid biochemistry and molecular biology 07/2009; 117(1-3):74-80. · 2.66 Impact Factor
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ABSTRACT: The purpose of this study was to investigate the large-scale characteristic molecular signature of Müllerian inhibiting substance (MIS) in human ovarian cancer cells through expression genomics. To understand the comprehensive molecular mechanisms by which MIS inhibits ovarian cancer cell growth, we identified the large-scale characteristic molecular changes elicited by MIS in the human ovarian cancer cell line OVCAR-8, using DNA microarray analysis. Combined serial gene expression analysis from 0 to 96 h after MIS treatment of OVCAR-8 cells resulted in 759 genes which showed at least a 2-fold change in overexpression or underexpression compared to non-treatment groups. Of the 759 outlier genes, 498 genes were mapped to known biological cellular processes, and the resultant major pathways included metabolism, signal transduction, cell growth and apoptosis. Among these pathways, 68 genetic elements were dissected as cell cycle-related genes induced by MIS. Although cellular phenotypic changes by MIS were observed after 24 h of treatment, the characteristic large-scale molecular changes were observed from 48 to 96 h of exposure to MIS. This finding may imply that the suppressive role of MIS on ovarian cancer cells could be cumulative in that the metabolic disturbance of MIS is followed by arrest at the G1/S cell cycle checkpoint. We suggest 759 outlier genes comprise the characteristic molecular signature of MIS, which may be responsible for the suppressive effect on OVCAR-8 cells. Although the precise biological mechanisms underlying these outlier genes should be validated, the genetic elements described herein provide promising therapeutic interventions for ovarian cancer.
International Journal of Molecular Medicine 06/2009; 23(5):589-96. · 1.98 Impact Factor
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ABSTRACT: This study investigated the expression patterns of Müllerian inhibiting substance/anti-Müllerian hormone type II receptor (MIS/AMHRII) and mRNA in various types of ovarian neoplasia and evaluated the clinical significance of MIS/AMH as a biological response modifier for MIS/AMHR-positive tumors. Reverse transcriptase polymerase chain reaction was used to detect MIS/AMHRII mRNA expression and in situ hybridization and immunohistochemistry were used to localize MIS/AMHRII mRNA and protein expression. The degree of expression was scored from 0 (no staining) to 3 (strong staining). There was no significant difference in expression intensity between MIS/AMHRII protein and mRNA on all ovarian samples whether benign or malignant. MIS/AMHRII protein and mRNA were weakly expressed on 45.45% of benign ovarian tumors. In borderline tumors, expression rates of MIS/AMHRII protein and mRNA were 77.78% with score 1.22 and 55.56% with score 1, respectively. In malignant ovarian tumors, expression rates of MIS/AMHRII protein and mRNA were 70% with score 1.23 and 75% with score 1.43, respectively. Among malignant ovarian tumors, sex cord stromal tumors showed the highest expression rate and the strongest intensity of MIS/AMHRII protein and mRNA followed by germ cell tumor and epithelial ovarian tumor. Non-epithelial malignant tumors showed stronger expression than that of epithelial tumors (P<0.05, P<0.001, respectively). In serous borderline malignant and malignant tumors, MIS/AMHRII protein and mRNA expression was 63.64 and 81.82% with expression intensity of 1.27 and 1.46, respectively, which were not statistically different from non-epithelial malignant tumors. MIS/AMHRII and MIS/AMHRII mRNA demonstrate significantly variable expression among different ovarian tumor types. Non-epithelial cell tumors show higher expression than those of epithelial cell tumors. The highest expression rate and intensity were observed on sex cord stromal tumors. MIS/AMHRII expression was not different according to the differentiation, but showed tissue-type specificity. These data support that MIS/AMH may be used as a biological modifier or therapeutic modulator in MIS/AMHRII-expressed ovarian tumors.
International Journal of Oncology 06/2009; 34(6):1583-91. · 2.40 Impact Factor
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ABSTRACT: Schwannoma (neurilemmoma) is a peripheral nerve sheath tumor and commonly occurs singularly on the head, neck, and trunk. Giant schwannoma is rarely located on the retroperitoneum and pelvic cavity. The majority of symptoms caused by the tumor are due to the effect of its mass. Surgical resection is enough to treat the tumor. Schwannoma is reported usually as benign, and despite incomplete resection of the tumor, the risk of recurrence and metastasis is low. A schwannoma on the retroperitoneum that was preoperatively misdiagnosed as a malignant adnexal mass in a 60-year-old menopausal woman is presented, with a brief review of the literature.
Journal of Obstetrics and Gynaecology Research 07/2007; 33(3):371-5. · 0.94 Impact Factor
