Healthy women and patients with endometriosis show high concentrations of inhibin A, inhibin B, and activin A in peritoneal fluid throughout the menstrual cycle

Florio, Pasquale; Luisi, Stefano; Viganò, Paola; Busacca, Mauro; Fadalti, M; Genazzani, Ar; Petraglia, Felice

doi:10.1093/humrep/13.9.2606

Cited by 40 publications

(23 citation statements)

References 30 publications

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“…The authors (26) also demonstrated that the inhibin A and activin A concentrations in the cystic fluid of ovarian endometriosis were significantly higher than in the peripheral blood using a two-site enzyme immunoassay. On the other hand, Florio et al (27) reported that cultured endometriotic cells expressed the mRNA of inhibin ·-, ßA-, ßB-subunits, and activin receptors types II and IIB, and that the inhibin A, inhibin B and activin A concentrations of the peritoneal fluid were not significantly different between healthy women and patients with endometriosis. Cobellis et al (28) also reported that no significant difference was observed in the peritoneal fluid activin A concentrations between patients with endometriosis and healthy controls.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical localization of inhibin and activin subunits, activin receptors and Smads in ovarian endometriosis

Mabuchi

Yamoto²,

Minami³

et al. 2009

Int J Mol Med

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Abstracts. We previously reported that activin A, not inhibin, was localized to endometrial tissues, and that the endometrium might be a major source of activin A during the menstrual cycle, using an immunohistochemical method. However, there are few detailed reports concerning the expression of inhibin subunits, activin receptors and Smad proteins in the ectopic endometrial tissues of endometriosis. In this study, our purpose was to evaluate the immunohistochemical localization of inhibin ·-, ßA-subunits, activin A, activin receptor, and Smad proteins in ovarian endometriosis. Tissue samples from ovarian endometriosis were obtained from 13 women. Normal endometrial tissues were obtained during the proliferative phase from 5 premenopausal women without endometriosis who were undergoing a hysterectomy for the treatment of uterine cervical intraepithelial neoplasia 3. We examined the immunohistochemical localization of inhibin/activin ·-, ßA-subunit, activin A, activin receptors types IA, IB, IIA, IIB, Smad2, Smad3 and Smad4 using an avidin-biotin-peroxidase complex technique. No immunostaining for the ·-subunit of inhibin was observed in ovarian endometriosis and the normal endometrium. Positive immunostaining for the ßA-subunit of inhibin, activin A, activin receptors types IA, IB, IIA, IIB, Smad2, Smad3 and Smad4 was observed in ovarian endometriosis and the normal endometrium. In conclusion, these results suggest that activin A, but not inhibins, is produced by ovarian endometriosis and the normal endometrium, and that the activin signal transduction system exists in both ovarian endometriosis and the normal endometrium.

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Section: Discussionmentioning

confidence: 99%

Immunohistochemical localization of inhibin and activin subunits, activin receptors and Smads in ovarian endometriosis

Mabuchi

Yamoto²,

Minami³

et al. 2009

Int J Mol Med

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“…In the present study, the peritoneal fluid concentrations of all inhibins far exceeded the corresponding serum values. High peritoneal fluid concentrations of both total inhibin and dimeric inhibin have previously been measured in fertile-aged healthy women and in those with endometriosis (19,27,28). Little, if anything, is known about peritoneal fluid concentrations of inhibins in postmenopausal women, and no normal range has been determined previously.…”

Section: Discussionmentioning

confidence: 99%

“…The function of pro-aC has not yet been ascertained, but its serum concentrations are known greatly to exceed those of inhibins A and B (13,18). Few data are available as to which molecular forms of inhibins are secreted into the circulation by different types of ovarian tumors (5,(11)(12)(13)(14), and the role and function of inhibins in the peritoneal fluid have not yet been clarified (19). Recent studies suggest that the a-subunit, rather than the dimeric forms, are increased in epithelial ovarian carcinomas, whereas ovarian granulosa cell tumors preferentially secrete dimeric inhibins (13,14).…”

Section: Introductionmentioning

confidence: 99%

Inhibin A, B and pro-alphaC in serum and peritoneal fluid in postmenopausal patients with ovarian tumors

Ala-Fossi

Mäenpää

Bläuer³

et al. 2000

European Journal of Endocrinology

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Objective: To compare serum and peritoneal fluid concentrations of inhibin A, B, and pro-aC in women with ovarian tumors. Methods: Serum and peritoneal fluid samples were taken from 41 postmenopausal women operated on for an ovarian tumor. Twenty-one patients with endometrial cancer formed a control group. Serum and peritoneal fluid inhibin A, B, and pro-aC concentrations, and serum FSH and tumor marker CA 125 (study group only) concentrations were analyzed. Results: Inhibin A was found in low concentrations (median 4.1 pg/ml, range < 2-29 pg/ml) in serum in most postmenopausal patients with epithelial ovarian carcinoma, whereas inhibin B was not measurable. Inhibin pro-aC circulated in high concentrations (median 125 pg/ml, range 37->1000 pg/ml). All inhibins were found in clearly greater concentrations in the peritoneal fluid than in serum. International Federation of Gynecology and Obstetrics (FIGO) stage III-IV and poor differentiation grade were associated with significantly lower concentrations of inhibin A and proaC in the peritoneal fluid compared with stages I-II or low grade. This correlation was not found in the serum concentrations of inhibin A or pro-aC. In the control group, no dimeric inhibins were found in serum, and pro-aC circulated in median concentrations of 47 pg/ml (range 12-174 pg/ml). Conclusions: Postmenopausal patients with epithelial ovarian tumors had low concentrations of inhibin A and relatively high concentrations of inhibin pro-aC in serum. The peritoneal fluid concentrations of all inhibins far exceeded those in the serum. Relatively low concentrations of inhibin A and pro-aC in the peritoneal fluid of patients with ovarian cancer seem to be associated with high stage and grade and, to a lesser degree, with positive peritoneal cytology.

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“…During organogenesis, both olfactory and GnRH neurons originate in the olfactory placode that will eventually give rise to the olfactory epithelium. Although the olfactory cells project their axons to the olfactory bulb, the GnRH neurons migrate along the pathway of the olfactory nerve, cross the nasal septum and arrive at the septal± preoptic area and hypothalamus (21,22). Therefore, the targeting of the olfactory axons and the migration of the GnRH neurons appear to be time-correlated (23,24); thus, olfactory neurons and GnRH neurons have a common origin during organogenesis (21,22).…”

Section: Discussionmentioning

confidence: 99%

Human GnRH-secreting cultured neurons express activin betaA subunit mRNA and secrete dimeric activin A

Florio

Vannelli²,

Luisi³

et al. 2000

European Journal of Endocrinology

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Objective: To evaluate the expression of activin bA-subunit mRNA and the secretion of activin A in/from cultured GnRH-secreting neuronal cells cloned from human olfactory epithelium (FNC-B4), which showed biochemical and antigenic properties of GnRH-secreting neurons. Design: FNC-B4 cells were cultured in basal and conditioned media. Methods: Reverse transcription-polymerase chain reaction (RTR±PCR) evaluated the expression of activin bA-subunit mRNA. By using a speci®c ELISA, dimeric activin A concentrations were measured in culture media, in the absence or presence of carvone or forskolin and with different doses of progesterone, GnRH, and estradiol. Results: RT±PCR experiments performed on total RNA isolated from FNC-B4 cells, using speci®c primers for the activin bA gene, showed a 787 bp DNA band corresponding to the bA gene. FNC-B4 cells secreted activin A, and the highest accumulation in conditioned medium was achieved after 3 h culture: the addition of forskolin, but not of carvone, was able to stimulate the release of activin A from cultured neuronal cells (P < 0.01). When progesterone or GnRH was added, a signi®cant accumulation of activin A was observed (P < 0.01), while estradiol administration did not signi®cantly affect activin A secretion. Conclusion: To date, this is the only study, in an in vitro human model reporting, that GnRH-secreting neuronal cells expressed activin bA-subunit mRNA, and released dimeric activin A in culture medium. The expression and secretion of activin suggests that in these cells activin A might exert its action by autocrine/paracrine mechanisms.

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Healthy women and patients with endometriosis show high concentrations of inhibin A, inhibin B, and activin A in peritoneal fluid throughout the menstrual cycle

Cited by 40 publications

References 30 publications

Immunohistochemical localization of inhibin and activin subunits, activin receptors and Smads in ovarian endometriosis

Immunohistochemical localization of inhibin and activin subunits, activin receptors and Smads in ovarian endometriosis

Inhibin A, B and pro-alphaC in serum and peritoneal fluid in postmenopausal patients with ovarian tumors

Human GnRH-secreting cultured neurons express activin betaA subunit mRNA and secrete dimeric activin A

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