期刊
GENERAL AND COMPARATIVE ENDOCRINOLOGY
卷 273, 期 -, 页码 3-10出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ygcen.2018.02.003
关键词
Efferent ductules; Epididymis; Cell proliferation; Apoptosis; Seasonality; Chiroptera
资金
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico - CNPq/Brazil
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior - CAPES/Brazil
The balance between cell proliferation and apoptosis is important for maintenance of male fertility, being influenced by a variety of stimuli including androgens and estrogens. However, studies concerning regulation of these processes along the male reproductive tract under physiological conditions are scarce. Therefore, in this study, we investigated the profile of cell proliferation and apoptosis in the efferent ductules and epididymis of the Neotropical bat Artibeus lituratus, a seasonal breeder that presents natural variation in components of the androgen and estrogen responsive systems along the circannual cycle. Low rates of cell proliferation and apoptosis were found in the efferent ductules and epididymis of A. lituratus during the reproductive period, as few epithelial cells were positive for MCM7 (proliferation marker) and cleaved caspase-3 or TUNEL (apoptosis markers). In contrast, during the regressive period, the rate of both proliferating and apoptotic cells was significantly higher in the epithelium lining the efferent ductules as well as throughout the epididymis. The increased proliferative activity at this phase was positively correlated with the expression of estrogen receptor alpha (ER alpha), whereas the variation in apoptosis appears to be unrelated to the local expression of androgen and estrogen receptors. Together, these data suggest that cell proliferation and apoptosis are differentially modulated in the efferent ductules and epididymis of A. lituratus during the annual reproductive cycle, and support the hypothesis that ERa may be important in preparing the male reproductive tract for sexual recrudescence. (C) 2018 Elsevier Inc. All rights reserved.
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