Cell and tissue research · 2004
Regulation of the initial segment of the murine epididymis by dihydrotestosterone and testicular exocrine secretions studied by expression of specific proteins and gene expression.
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Avram C, Yeung C-H, Nieschlag E, Cooper T G
Аннотация
The murine caput epididymidis responded to deprivation of luminal fluid from the testis by regression of the initial segment but maintenance of the adjacent proximal and distal caput regions, as judged by immunohistochemical staining of the glutamate transporter EAAC1 and the lipocalin MEP17 and enzymatic activity of beta-galactosidase (beta-Gal). Additional removal of circulating androgens by bilateral castration similarly led to loss of the initial segment and of the proximal caput but the distal caput was transformed into an epithelium containing more apical than principal cells staining for EAAC1; this epithelium resembled the precursor epithelium usually only seen in prepubertal juveniles. Administration of dihydrotestosterone (DHT) to the castrates maintained the proximal and distal caput epithelia and induced a proximal epithelium, which resembled the initial segment in its prominent staining for Golgi, EAAC1 and beta-Gal activity, although it was short and exhibited no MEP17 expression. DHT was present in the c-ros knockout caput epididymidis lacking the initial segment and in the heterozygous organ but the DHT concentration was lower in the knockout corpus. The maintenance of the full complement of epithelia in the murine caput epididymidis in the adult thus requires a combination of luminal fluid from the testis, tissue DHT and the presence of the c-ros oncogene.
Предметные рубрики MeSH
Amino Acid Transport System X-AGAndrogensAnimalsBody WeightCarrier ProteinsCastrationDihydrotestosteroneEpididymisExcitatory Amino Acid Transporter 3Gene Expression RegulationGlutamate Plasma Membrane Transport ProteinsLigationLipocalinsMaleMiceMice, Inbred C57BLMice, KnockoutOrgan SizeProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesSymportersTesticular Hormonesbeta-Galactosidase