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Presence of neuroendocrine cells during postnatal development in rat prostate: Immunohistochemical, molecular, and quantitative study
Author(s) -
Rodríguez Rosario,
Pozuelo José M.,
Martín Rocío,
HenriquesGil Nuno,
Haro María,
Arriazu Riánsares,
Santamaría Luis
Publication year - 2003
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.10287
Subject(s) - chromogranin a , immunohistochemistry , prostate , endocrinology , medicine , messenger rna , biology , gene , cancer , biochemistry
Abstract BACKGROUND This work was undertaken to study the prostate neuroendocrine cells (PNEC) during the post‐natal development of rats. METHODS Forty male Wistar rats (pre‐pubertals, pubertals, young, and aged adults) were used for immunohistochemistry of chromogranin A (cgA), serotonin (SER), and protein gene product 9.5 (PGP9.5). They were also evaluated for numerical cell density (N V SER) and PNEC number per prostate (N SER). Five additional young adult rats were used for a RT‐PCR study (mRNA cgA detection). RESULTS Weak immunoreactivity to cgA was observed in pubertal rats. No PNEC immunostained to PGP 9.5 was observed. Cells expressing SER were detected in all the groups exclusively located in periurethral ducts. The N V SER increased significantly in pubertal animals. In aged animals, it decreased to levels observed in pre‐pubertal rats. The N SER increased significantly from pre‐pubertal to young adults, decreasing in aged adults. There was weak production of cgA mRNA, with more expression in the dorsal prostate. CONCLUSIONS PNEC differ in rats when compared to humans: they are weakly immunopositive to cgA, do not express PGP 9.5, only show immunoreactivity to SER, and do not appear in acini. The changes in the amount of rat PNEC during the post‐natal development suggest an androgenic influx. PNEC might regulate the contractility of periurethral ducts. Prostate 57: 176–185, 2003. © 2003 Wiley‐Liss, Inc.