INVESTIGADORES
CARVELLI Flavia Lorena
congresos y reuniones científicas
Título:
Expression of proteins that regulate intracellular traffic is controlled by androgens in rat epididymis
Autor/es:
CARVELLI L; JOFRÉ G; BARRERA P; SARTOR T; SOSA MA
Lugar:
Pinamar (Buenos Aires)
Reunión:
Congreso; 41th Reunión Anual de la Sociedad Argentina de Investigación Bioquímica (SAIB); 2005
Institución organizadora:
Sociedad Argentina de Investigación Bioquímica y biología molecular
Resumen:
Mammalian epididymis provides the proper environment for sperm maturation thanks to the secretory activity of its epithelium. As occurs in other organs of male reproductive tract, epididymis is highly influenced by hormones, since androgen deprivation induces morphological and biochemical changes. The presence of high activities of acid hydrolases in epididymal lumen is still poorly understood, and these enzymes could play a role in sperm maturation. In other cell types, transport of these enzymes to lysosomes is regulated by specific receptors (MPRs) that recognize mannose-6-phosphate on the enzyme molecule. Two types of receptor have described so far, the cation-dependent (CD.MPR) and the cation-independent (CD-MPR), and little is known about the co-existence of both proteins in most of cell types. We wondered if MPRs participate in transport and secretion of acid hydrolases in rat epididymis and if they are influenced by hormonal changes. Regarding these questions, we measured expression of MPRs in epididymis of rats castrated or treated with the antiandrogenic drug Flutamide (Ft). By Western blot studies we observed that both CD- and CI-MPR expression is increased either in castrated or in Ft treated rats. However, no variations in mRNA levels were observed by RT-PCR, indicating that the effect could be post-transcriptional. We also observed an increased synthesis and secretion of cathepsin D, mostly as precursor of 54 kDa. We concluded that castration or treatment with Ft induces variations in transport and secretion of certain enzymes by changes in expression of MPRs.