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Postnatal Development of Transporter Proteins in Epididymal Clear Cells of Rhesus Monkey (Macaca mulatta)
Author(s) -
PastorSoler Nuria,
Smolak Christy,
Gong Fan
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1188.9
Subject(s) - epididymis , biology , rodent , vas deferens , cystic fibrosis transmembrane conductance regulator , microbiology and biotechnology , male infertility , transporter , endocrinology , infertility , medicine , sperm , cystic fibrosis , gene , genetics , pregnancy , ecology
Our understanding of human epididymal physiology is mostly based on rodent studies. However, only half of mouse epididymal genes have orthologs in humans. Moreover, unlike in rodents, androgen exposure in primates is interrupted between infancy and puberty. The epididymal clear cell marker vacuolar H + ‐ATPase (V‐ATPase) helps maintain a luminal acidic pH, which is essential for sperm maturation. We hypothesize that developmental expression of clear cell transporter proteins differs between rodents and rhesus. Such differences may be important in understanding human infertility. One‐week‐old rats already have V‐ATPase in clear cells, but we found that this transporter is not expressed until the juvenile stage in rhesus. We also found that adult rhesus epididymis expresses abundant V‐ATPase and carbonic anhydrase, another clear cell marker. In addition, as in human adult epididymis, we detected in rhesus clear cells the cystic fibrosis transmembrane conductance regulator (CFTR), a protein that is much less abundant in rodent clear cells. It is known that mild deficiencies in CFTR function can lead to severe epididymal/vas deferens pathology and infertility in humans. These results highlight the need to systematically investigate the development and physiology of rhesus, rather than rodent, epididymis as a model for understanding human epididymal function.