TRPM‐2 gene expression in normal rat ventral prostate following castration and exposure to diethylstilbestrol, flutamide, MK‐906 (finasteride), and coumarin Journal Article


Authors: Russo, P.; Warner, J. A.; Huryk, R.; Perez, G.; Heston, W. D. W.
Article Title: TRPM‐2 gene expression in normal rat ventral prostate following castration and exposure to diethylstilbestrol, flutamide, MK‐906 (finasteride), and coumarin
Abstract: TRPM‐2, not normally expressed in the rat ventral prostate, has been identified as an important genetic marker of castration‐induced apoptotic cell death. It is not known whether other agents capable of causing growth inhibition of the rat ventral prostate also induce TRPM‐2 expression. To investigate this further, 270 mature Sprague‐Dawley rats were randomized into one of six groups: control, castration, diethylstilbestrol (DES), flutamide, MK‐906 (finasteride), or coumarin. Five rats per group were sacrificed on days 1, 3, 5, 7, 10, and 21. Serum testosterone, body weights, and prostate weights were determined at each time point. The ventral prostate was removed and cellular RNA extracted. Northern blot analysis using cDNA probes for TRPM‐2 and γ‐actin were performed at each time point. Only DES significantly decreased rat weights. DES and castration reduced serum testosterone to undetectable levels by the next day. Flutamide caused a 3.0‐ to 4.5‐fold increase in serum testosterone above control. Coumarin and MK‐906 did not affect serum testosterone levels. DES and castration reduced prostate weights to 20% and 6% of control, respectively, while inducing TRPM‐2 expression to a maximum on day 5 of the experiment. DES induced TRPM‐2 expression over a longer duration than did castration, suggesting that more than just the decrease of serum testosterone to castrate levels plays a role in the expression of TRPM‐2. MK‐906, coumarin, and flutamide reduced prostatic weights to a lesser extent (50%, 63%, 71% of control, respectively), but these agents did not induce TRPM‐2 expression at any time during the experiment. TRPM‐2 expression in the rat ventral prostate does not correlate simply with catabolic effects on the prostate. © 1994 Wiley‐Liss, Inc. Copyright © 1994 Wiley‐Liss, Inc., A Wiley Company
Keywords: controlled study; nonhuman; animal cell; animal; animal tissue; cell death; apoptosis; animal experiment; estrogen therapy; body weight; gene expression regulation; prostate; rna, messenger; diagnosis; rat; finasteride; rats; diethylstilbestrol; flutamide; castration; orchiectomy; testosterone blood level; rats, sprague-dawley; hormonal regulation; testosterone; glycoproteins; genetic marker; genetic markers; oral drug administration; organ weight; coumarin; coumarins; intraperitoneal drug administration; programmed cell death; male; priority journal; article; support, non-u.s. gov't; support, u.s. gov't, p.h.s.; hormone manipulation; g actin; prostate ventral lobe
Journal Title: Prostate
Volume: 24
Issue: 5
ISSN: 0270-4137
Publisher: John Wiley & Sons  
Date Published: 1994-05-01
Start Page: 237
End Page: 243
Language: English
DOI: 10.1002/pros.2990240504
PROVIDER: scopus
PUBMED: 8170836
DOI/URL:
Notes: Export Date: 14 January 2019 -- Article -- Source: Scopus
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  1. Warren Heston
    136 Heston
  2. Paul Russo
    581 Russo
  3. Robert   Huryk
    28 Huryk