4.2 Article

Aberrantly increased mRNA expression of betaglycan, an inhibin co-receptor in the ovarian tissues in women with polycystic ovary syndrome

Journal

JOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH
Volume 36, Issue 1, Pages 138-146

Publisher

WILEY
DOI: 10.1111/j.1447-0756.2009.01103.x

Keywords

betaglycan; inhibin B; ovary; polycystic ovary syndrome; real-time PCR

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Aim: To compare the gene expressional levels of receptors for activins and inhibins in ovarian tissues between women with polycystic ovary syndrome (PCOS) and normal controls, and to analyze their biologically relevant associations with serum hormone levels. Methods: Total RNA of ovarian tissues from PCOS (n = 14) and normal controls (n = 21) were isolated during the follicular phase of the menstrual cycle. Real-time PCRs were performed to examine the relative mRNA expression levels of the activin receptors, including activin receptor type IA (ActRIA), type IB (ActRIB), type IIA (ActRIIA), and type IIB (ActRIIB), and the inhibin receptors, betaglycan and an inhibin binding protein (InhBP/p120). At the same time, the serum levels of estradiol (E-2), testosterone (T), follicle-stimulating hormone (FSH), luteinizing hormone (LH), inhibin B and activin A were measured. Results: The PCOS patients showed endocrine characteristics with higher concentrations of LH, T and inhibin B, and a lower concentration of activin A. Real-time PCR demonstrated that the relative expression level of betaglycan against that of GAPDH was increased 1.5-fold in the ovarian tissues during the follicular phase of PCOS patients when compared with normal controls, while the activin receptors ActRIA, ActRIB, ActRIIA, ActRIIB, and the inhibin co-receptor InhBP/p120 were unchanged. Moreover, the betaglycan mRNA expression showed biologically relevant associations with serum FSH, LH, E-2 and inhibin B levels in both the PCOS and normal controls. Conclusions: This is the first report to demonstrate the aberrantly increased expression of betaglycan mRNA in PCOS ovaries. The mechanism by which betaglycan contributes to the pathologic process of PCOS remains to be clarified.

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