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Sperm storage in the female reproductive tract of Scotophilus heathii : Role of androgen
Author(s) -
Roy Vikas Kumar,
Krishna Amitabh
Publication year - 2011
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.21328
Subject(s) - biology , sperm , reproductive biology , reproductive tract , zoology , androgen , female reproductive tract , physiology , andrology , endocrinology , microbiology and biotechnology , genetics , hormone , embryogenesis , embryo , medicine
Abstract The aim of the present study was to investigate the mechanism of androgen‐mediated, prolonged sperm‐storage in the female reproductive tract of the bat, Scotophilus heathii . The bat treated in vivo with flutamide, an androgen antagonist, showed loss of spermatozoa at the storage site, utero‐tubal junction. Immunocytochemistry and Western blot analysis revealed the presence of increased expression of Bcl2 in the epithelial cell lining of the utero‐tubal junction during the period of sperm‐storage. Treatment with testosterone in vitro caused a significant dose‐dependent increase in expression of the survival factor Bcl2, whereas treatment with flutamide together with testosterone caused a significant decline in Bcl2 in the utero‐tubal junction of S. heathii . Together with the expression of Bcl2, the utero‐tubal junction also expresses the death signal, caspase3. Expression of caspase3 decreased during January, but increased in February during the late stage of sperm storage. Androgen stimulated Bcl2 synthesis in the utero‐tubal junction via the non‐genomic MAP kinase signaling pathway. In conclusion, this study suggests that androgen promotes sperm storage in S. heathii by stimulating the survival factor Bcl2 in the utero‐tubal junction. It is further hypothesized that a balance between the survival factor, Bcl2, and the death signal, caspase3, determines the duration of sperm storage in S. heathii . Mol. Reprod. Dev. 78:477–487, 2011. © 2011 Wiley‐Liss, Inc.