Biomedical subjects

Mareo Yamoto

Publications and source records attributed to Mareo Yamoto.

6 recordsLinked to original sources

PubMed2006

Immunohistochemical localization of inhibin and activin subunits, activin receptors, and Smads in ovarian clear cell adenocarcinoma.

Our purpose was to examine the immunolocalization of inhibin, activin and the activin signaling system in ovarian clear cell adenocarcinoma tissue. Tissue samples of ovarian clear cell adenocarcinoma were collected from ten women. The patients' ages ranged from 41 to 71 years (mean +/- standard deviation; 53.4+/-9.9). Their surgicopathological staging was based on the criteria of the International Federation of Gynecology and Obstetrics (FIGO); there were 5 patients with stage I, 3 with stage II, and 2 with stage III. We examined the immunohistochemical localization of inhibin/activin alpha-subunit, betaA-subunit, activin A, and activin receptor types IA, IB, IIA, IIB, Smad2, Smad3 and Smad4 using an avidin-biotin peroxidase complex technique. With the antibodies against the betaA-subunit, and activin A, we observed positive immunoreactive staining in the cytoplasm of clear cell adenocarcinoma, whereas we did not observe any staining for the alpha-subunit of inhibin. We observed positive immunoreactive staining in the cell cytoplasm and surface with the antibodies against the activin receptors, types IA, IB, IIA and IIB. We observed positive immunoreactive staining in the cytoplasm and nucleus with the antibodies against the Smad2, Smad3 and Smad4. It is suggested that activin A, not inhibins, might be secreted by ovarian clear cell adenocarcinoma, and that an activin signal transduction pathway might exist in ovarian clear cell adenocarcinoma.

Activin Receptors↗

PubMed2006

The autocrine effect of activin A on human ovarian clear cell adenocarcinoma cells.

The functions of activin, a member of TGF-beta superfamily, in ovarian clear cell adenocarcinoma remain unsolved, although we recently found that inhibin betaA-subunit, activin A, activin receptor type IA, type IB, type IIA, type IIB, Smad2, Smad3 and Smad4 were localized in tumor cells of the ovarian clear cell adenocarcinoma tissue by immunohistochemistry. In the present study, in order to investigate the role of activin concerning cell growth in ovarian clear cell adenocarcinoma cells, we determined the production of activin A and inhibin A, and the expression of activin receptors and Smads using the human ovarian clear cell adenocarcinoma cell line JHOC-5. Moreover, we examined the effects of activin A on the activation of activin signaling pathway and on the proliferation in JHOC-5 cells. We detected a measurable amount of activin A in the culture medium of JHOC-5 cells, although inhibin A was not detected. The expression of activin receptor type IA, IB, IIA, IIB, Smad2, Smad3 and Smad4 was observed in JHOC-5 cells. Activin A induced a significant increase in proliferation of JHOC-5 cells compared with the untreated control. On the other hand, activin A did not affect the growth of JHOC-5 cells and no statistically significant difference was observed in the presence of follistatin which is a specific binding protein of activin. Phosphorylated Smad2, an activated form of Smad2, was detected both in treated JHOC-5 cells and in untreated cells by activin A. Activin A significantly increased the expression of phosphorylated Smad2 in JHOC-5 cells. Therefore, it is possible that activin has autocrine roles in tumor growth of ovarian clear cell adenocarcinoma cells.

Activin Receptors↗

PubMed2005

[Inhibin].

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Biomarkers↗

PubMed2003

Expression and function of activin receptors in human endometrial adenocarcinoma cells.

Menstrual cycle-dependent expressions of activin A in normal human endometrial tissues have been reported. Expression of activin receptor mRNAs and increased activin A production were also observed in human endometrial adenocarcinoma tissues, suggesting that activin A might enhance cell proliferation and inhibit apoptotic signaling in endometrial cancer cells. In this study, we have examined the effects of activin A on cell proliferation, anticancer drug-induced apoptosis and Fas-mediated apoptosis in 3 differentiated human endometrial adenocarcinoma cell lines, namely HEC-1, HHUA and Ishikawa. Flow cytometric analyses revealed moderate expressions of all 4 types of activin receptor subunits on the cell surfaces of the 3 cell lines. The proliferations of the 3 endometrial cancer cells were completely unaffected by activin A, whereas it suppressed the cell proliferation of a human ovarian endometrioid adenocarcinoma cell line, OVK-18, in a dose-dependent manner. Moreover, activin A did not affect the apoptotic changes in the 3 endometrial adenocarcinoma cells treated with 4 different anticancer drugs, namely CDDP, paclitaxel, etoposide and SN38. The apoptotic changes in HHUA cells treated with anti-Fas IgM were also unaffected by activin A. These results indicate that the increased activin A production in human endometrial adenocarcinoma tissues in vivo may not stimulate carcinoma cell proliferation or inhibit apoptotic signaling in carcinoma cells. Insensitivity to the usual growth suppression signals induced by activin A might be one of the mechanisms of immortality of human endometrial adenocarcinoma cells.

Activin Receptors↗

PubMed2002

Postmenopausal intravenous leiomyomatosis with high levels of estradiol and estrogen receptor.

BACKGROUND: Intravenous leiomyomatosis is a rare variant of leiomyoma. CASE: The patient was a 49-year-old gravida 3, para 3 woman with menopause at age 46. She presented with a history of syncope. Vaginal examination revealed an enlarged and elastic-soft mass of the uterus. A pelvic ultrasound, computed tomography scan, and magnetic resonance imaging showed a heterogeneous, irregularly shaped 8- to 10-cm tumor. In addition, the inferior vena cava was almost completely occluded. Cardiac ultrasound demonstrated a mobile mass in the right atrium. The serum estradiol was 208 pg/mL (normal 0-59). Intravenous leiomyomatosis with cardiac extension was diagnosed preoperatively. A resection of the intracardiac and intracaval mass and a subtotal hysterectomy with bilateral salpingo-oophorectomy were performed. The uterine tumor weighed 600 g, and the cordlike intravascular tumor extending from the internal iliac vein into the right ventricle was 40 cm long and weighed 60 g. Pathologic examination confirmed intravenous leiomyomatosis with no evidence of atypia. The level of estrogen receptor in the tissue was 140 fmol/mg protein. The postoperative course was uneventful, and she has been in good health for 17 months after the operation. CONCLUSION: We report a case of intravenous leiomyomatosis extending into the right ventricle treated with a one-stage operation. It is possible that a high concentration of serum estradiol and high level of tissue estrogen receptor are related to the intravenous leiomyomatosis.

Estradiol↗

PubMed2002

[Mutations in the follicle-stimulating hormone receptor genes in patients with gonadal dysfunction].

Follicle-stimulating hormone(FSH) plays important roles in gametogenesis and steroidogenesis in human gonads. Both activating and inactivating mutations have been detected only a few number in the gene for the FSH receptor. Inactivating mutations in the gene for the FSH receptor are involved in some female patients of hypergonadotropic hypogonadism with infertility. Only one activating mutation of FSH receptor was reported to have fertile functions in a hypophysectomized man. This article describes the reported genetic alterations of FSH receptor in humans and reviews how help us to understanding the molecular biology in the pathogenesis of gonadal dysfunction.

Female↗