Hyaluronan content and distribution in the rat ventral prostate after castration

Abstract

Hyaluronan (HA) has been implicated in tissue remodeling, healing, and tumor growth. This study investigated the variation in hyaluronan content, distribution, and metabolism in the rat ventral prostate (VP) in response to androgen deprivation after castration. The mRNA abundance of hyaluronan synthases (Has1-3) and hyaluronidases (Hyal 1-3) were assessed by reverse transcription (RT)-PCR and immunohistochemistry, respectively. The results demonstrated an increased concentration, but an overall reduction in HA content. HA was located in both epithelium and stroma of the prostate of both the noncastrated and castrated animals. Quantitative RT-PCR (qRT-PCR) showed that Has1 and Has2 are major synthases, and that Hyal 1 was the predominant hydrolase expressed in the VP. qRT-PCR also showed that Has1 and Has2 mRNA increased transiently after castration, whereas Has3 mRNA declined markedly. While Hyal 1 mRNA increased slowly up to day 21 after castration, Hyal 2 and Hyal 3 mRNA dropped significantly. CD44 was found in the epithelial cells and in some stromal cells in both hormonal conditions. In conclusion, castration results in increased abundance of Has1 and Has2 mRNA, but is associated with a decrease in the total content of HA, with an increased concentration, and a predominance of short-chain HA molecules.

Proteoglycans orchestrate remodeling of prostatic cytoarchitecture after androgenic blockade in old gerbils

“…In guinea pigs, the highest rates of immunoreactive chondroitin were found in castrated animals, where staining of the periglandular basement membranes was uniformly intense. 35 In rat ventral prostate, a transient increase in high-molecular-mass hyaluronan was observed at 7 days after castration, 36 whereas an apparent increase in heparan sulfate content was observed at 21 days after the androgenic blockade. 37 In diabetic rats, an increase in chondroitin sulfate in the prostate was also influenced by the reduction in androgens caused by this condition.…”