Activin over-expression in the testis of mice lacking the inhibin α-subunit gene is associated with androgen deficiency and regression of the male reproductive tract. (15th July 2018)

• Record Type: Journal Article
• Authors: Wijayarathna, Rukmali; de Kretser, David M.; Meinhardt, Andreas; Middendorff, Ralf; Ludlow, Helen; Groome, Nigel P.; Loveland, Kate A.; Hedger, Mark P.
• Is Part Of: Molecular and cellular endocrinology. Volume 470(2018)
• Page Start: 188
• Page End: 198
• Publication Date: 2018-07-15
• Subjects: Activin -- Follistatin -- Inhibin -- Epididymis -- Vas deferens -- Androgens; Endocrinology -- Periodicals; Molecular biology -- Periodicals; Cytology -- Periodicals; Endocrinology -- Periodicals; Hormones -- Periodicals; Endocrinologie -- Périodiques; Cytology; Endocrinology; Molecular biology; Periodicals; 573.4
• DOI: 10.1016/j.mce.2017.10.013
• Languages: English
• ISSNs: 0303-7207

Abstract

Abstract: Regionalised interaction of the activins, follistatin and inhibin was investigated in the male reproductive tract of mice lacking the inhibin α-subunit ( Inha −/- ). Serum and intratesticular activin B, although not activin A and follistatin, were increased in Inha −/- mice at 25 days of age, but all three proteins were elevated at 56 days. None of these proteins were altered within the epididymis and vas deferens at either age. At 25 days, histology of the epididymis and vas deferens was similar to wild-type. At 56 days, the testis contained extensive somatic cell tumours, leading to Leydig cell regression and testosterone deficiency. The epididymis and vas deferens showed epithelial regression and increased prominence of the interstitial stroma. Immunoregulatory and fibrotic gene expression in the epididymis and vas deferens were unchanged. Thus, absence of the inhibin α-subunit has marginal effects on activins in the epididymis and vas deferens, and regression of these tissues is associated with androgen deficiency. Highlights: Activins are not significantly increased in the epididymis and vas deferens of Inha −/- mice. This contrasts with the large increase of testicular and systemic activins and follistatin. Adult Inha −/- mice are androgen deficient due to loss of Leydig cells. Regression of the epididymis and vas deferens is consistent with androgen deficiency.