Rat estrogen receptor-alpha and -beta, and progesterone receptor mRNA expression in various prostatic lobes and microdissected normal and dysplastic epithelial tissues of the Noble rats
UMass Chan Affiliations
Department of Surgery, Division of UrologyDepartment of Pathology
Graduate School of Biomedical Sciences
Document Type
Journal ArticlePublication Date
1998-01-08Keywords
Animals; Dissection; Estradiol; Gene Expression Regulation; Male; Prostate; RNA, Messenger; Rats; Receptors, Estrogen; Receptors, Progesterone; TestosteroneLife Sciences
Medicine and Health Sciences
Metadata
Show full item recordAbstract
Semiquantitative RT-PCR was used to determine if transcripts of the two estrogen receptor (ER) subtypes, ER alpha and ER beta, and the progesterone receptor (PR) are differentially expressed and/or regulated in the various normal lobes of the Noble (NBL) rat prostate. We found that ER beta mRNA was present at comparable, high levels in all three major prostatic lobes: dorsal (DP), lateral (LP) and ventral (VP) prostate. ER alpha mRNA was, however, expressed at low levels among the various lobes in the following descending order of abundance: LP>DP>VP. Expression of PR transcript was low and paralleled the expression pattern of ER alpha mRNA. Treatments of rats with testosterone (T) plus estradiol-17beta (E2) (T+E2) or T alone induced no discernible alterations in ER alpha, ER beta, and PR mRNA levels in the VP, DP and LP, while those with E2 caused a general decline in the expression of all three transcripts. We then studied the expression of the three receptors in the normal and dysplastic epithelium of the dorsolateral prostates (DLPs) of rats treated with T+E2. Comparable levels of ER beta mRNA were found in microdissected dysplastic and normal epithelia. In contrast, significantly higher levels of PR mRNA were present in epithelial samples from dysplastic acini. ER alpha mRNA was not detected in any of the microdissected epithelial samples. Results from this study suggest that upregulation of PR mRNA expression, likely mediated via ER beta action, is involved in the genesis of T+E2-induced dysplasia in this animal model.Source
Endocrinology. 1998 Jan;139(1):424-7.
DOI
10.1210/endo.139.1.5809Permanent Link to this Item
http://hdl.handle.net/20.500.14038/33993PubMed ID
9421443Related Resources
ae974a485f413a2113503eed53cd6c53
10.1210/endo.139.1.5809