Luteinizing hormone regulates seasonal steroidogenesis locally in the prostate of the muskrat (Ondatra zibethicus).
Luteinizing hormone may regulate local steroidogenesis in the prostate of muskrats, with HCG treatment promoting hormone secretion in vitro.
Where it sits
this study against the rest of the hcg (human chorionic gonadotropin) corpusSummary and findings
This study investigated the role of luteinizing hormone in regulating steroidogenesis in the prostate of muskrats during breeding and non-breeding seasons. The research involved histology, immunohistochemistry, RT-qPCR, and hormone assays. Human chorionic gonadotropin (HCG) treatment in vitro promoted the expression of luteinizing hormone receptor and steroidogenic enzymes, increasing testosterone and dihydrotestosterone secretion.
Abstract
The prostate is one of the important androgen-dependent organs in the male reproductive system. Although its ability for local steroid hormone synthesis is recognized, the regulatory mechanisms, particularly the role of hormones and the seasonal steroidogenesis expression within the tissue, remain unclear. This study investigated the phenomenon in the seasonal breeder muskrat (Ondatra zibethicus) by comparing breeding (B) and non-breeding (NB) season prostates through histology, immunohistochemistry (IHC), RT-qPCR, and hormone assays. Anatomy shows that the prostate is markedly enlarged during the breeding season. Immunohistochemistry revealed a marked cellular compartmentalization: luteinizing hormone receptor (LHR), steroidogenic acute regulatory protein (StAR), and Steroid 5-alpha-reductase 2 (SRD5A2) were predominant in epithelial cells, whereas cytochrome P450 family 11 subfamily A member 1 (P450scc) and steroid 17 alpha-hydroxylase (P450c17) were primarily localized to stromal cells. The gene expression of the steroidogenesis pathway was coordinately upregulated in the breeding season, and largely downregulated in the non-breeding season, which was further validated at the protein level by Western blot analysis showing significantly higher expression of LHR, P450scc, SRD5A2, and androgen receptor (AR) in the breeding season compared to the non-breeding season. The prostate in the breeding season contained higher levels of intra-tissue testosterone (T) and dihydrotestosterone (DHT). To investigate the underlying mechanism, we performed in vitro experiments using primary cultured muskrat prostate cells. Furthermore, in vitro experiments demonstrated that human chorionic gonadotropin (HCG) treatment promoted the expression of LHR and steroidogenic enzymes and elevated the secretion of T and DHT into the culture media. This induction was inhibited by the Protein Kinase A (PKA) inhibitor H89, which also abolished the HCG-induced increase in T and DHT secretion. H89 pre-treatment abolished the HCG-induced upregulation, confirming the presence of the LH-PKA pathway regulating steroidogenesis in the prostate. Taken together, our results reveal that LH-mediated activation of local steroidogenesis may regulate the seasonal growth of prostates in male muskrats.
Background
The regulation of steroid hormone synthesis in the prostate is not fully understood, particularly regarding seasonal changes. Previous studies have indicated that luteinizing hormone plays a role in steroidogenesis, but the specific mechanisms in seasonal breeders like the muskrat have not been thoroughly investigated. This study aims to clarify these mechanisms and their implications for prostate growth.
Methods
This research utilized histology, immunohistochemistry, RT-qPCR, and hormone assays to compare the prostates of muskrats during breeding and non-breeding seasons. The study involved primary cultured muskrat prostate cells to assess the effects of HCG on steroidogenic enzyme expression and hormone secretion. Specific doses and durations were not reported in the abstract.
Results
The study found that the prostate was significantly enlarged during the breeding season. There was a marked increase in the expression of key steroidogenic proteins and hormones during this period. HCG treatment in vitro resulted in increased expression of LHR and steroidogenic enzymes, along with elevated testosterone and dihydrotestosterone secretion.
Interpretation
These findings support the hypothesis that luteinizing hormone regulates local steroidogenesis in the prostate, particularly during the breeding season. However, the clinical significance of these results is uncertain due to the animal model used and the absence of direct human data. The study's reliance on in vitro methods also raises questions about the applicability of the findings to in vivo conditions.
Key findings
- Prostate significantly enlarged during the breeding season.
- Higher expression of LHR, P450scc, SRD5A2, and AR in breeding season compared to non-breeding season.
- Intra-tissue testosterone and dihydrotestosterone levels were higher in breeding season.
- HCG treatment promoted expression of LHR and steroidogenic enzymes.
- H89 pre-treatment abolished HCG-induced upregulation of steroidogenic enzymes.
Limitations
- Limited to muskrat model, not human data.
- In vitro findings may not reflect in vivo conditions.
- Small sample size not specified in abstract.
- Short duration of in vitro experiments.
- Potential confounding factors not addressed.