PMID- 16245307
OWN - NLM
STAT- MEDLINE
DCOM- 20060421
LR  - 20131121
IS  - 0021-9541 (Print)
IS  - 0021-9541 (Linking)
VI  - 206
IP  - 3
DP  - 2006 Mar
TI  - TNF-alpha-related apoptosis-inducing ligand decoy receptor DcR2 is targeted by 
      androgen action in the rat ventral prostate.
PG  - 709-17
AB  - The apoptotic cell death process in the prostate is known to be under the control 
      of androgens. Tumor necrosis factor-alpha (TNF-alpha)-related apoptosis-inducing 
      ligand (TRAIL) is a member of the TNF-alpha family of cytokines, known to induce 
      apoptosis upon binding to its death domain-containing receptors, DR4/TRAIL-R1 and 
      DR5/TRAIL-R2. Two additional TRAIL receptors, DcR1/TRAIL-R3 and DcR2/TRAIL-R4, 
      lack functional death domains and act as decoy receptors for TRAIL. In this 
      study, we examined whether TRAIL and cellular receptors expression was targeted 
      by androgens during the apoptotic cell death process in the hormone sensitive 
      ventral prostate. The role of androgens was investigated using two sets of 
      experiment. (1) Androgen deprivation associated with an apoptotic process 
      resulted in a decrease in DcR2 mRNA and protein expression in the ventral 
      prostate 3 days after castration. Testosterone administration to castrated adult 
      rats prevented the decrease in DcR2 mRNA and protein levels in the ventral 
      prostate. In contrast, DcR2 expression was modified, neither in the dorsolateral 
      nor in the anterior prostate following castration. No changes were observed in 
      DR4, DR5, DcR1, and TRAIL mRNA and protein levels in prostate after castration. 
      (2) A specific decrease in DcR2 expression was observed in the ventral prostate 
      after treatment of rats with the anti-androgen flutamide. Together, the present 
      results suggest that testosterone specifically controls DcR2 expression in the 
      adult rat ventral prostate. Androgen withdrawal, by reducing DcR2 expression, 
      might leave the cells vulnerable to cell death signals generated by TRAIL via its 
      functional receptors.
CI  - Copyright 2005 Wiley-Liss, Inc.
FAU - Vindrieux, David
AU  - Vindrieux D
AD  - Institut National de la Sante et de la Recherche Medicale, Communications 
      Cellulaires en Biologie de la Reproduction, Faculte de Medecine Lyon-Sud, Oullins 
      Cedex, France.
FAU - Reveiller, Marie
AU  - Reveiller M
FAU - Florin, Anne
AU  - Florin A
FAU - Blanchard, Cecile
AU  - Blanchard C
FAU - Ruffion, Alain
AU  - Ruffion A
FAU - Devonec, Marian
AU  - Devonec M
FAU - Benahmed, Mohamed
AU  - Benahmed M
FAU - Grataroli, Renee
AU  - Grataroli R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Androgen Antagonists)
RN  - 0 (Androgens)
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (TNF-Related Apoptosis-Inducing Ligand)
RN  - 0 (TNFSF10 protein, human)
RN  - 0 (Tnfsf10 protein, rat)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (decoy receptor 2, rat)
RN  - 3XMK78S47O (Testosterone)
RN  - 76W6J0943E (Flutamide)
SB  - IM
MH  - Androgen Antagonists/pharmacology
MH  - Androgens/*pharmacology
MH  - Animals
MH  - Apoptosis
MH  - Apoptosis Regulatory Proteins/*metabolism/physiology
MH  - Castration
MH  - Flutamide/pharmacology
MH  - HeLa Cells
MH  - Humans
MH  - Male
MH  - Membrane Glycoproteins/*metabolism/physiology
MH  - Prostate/cytology/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Tumor Necrosis Factor/genetics/*metabolism
MH  - Reproducibility of Results
MH  - TNF-Related Apoptosis-Inducing Ligand
MH  - Testosterone/pharmacology
MH  - Tumor Necrosis Factor-alpha/*metabolism/physiology
EDAT- 2005/10/26 09:00
MHDA- 2006/04/25 09:00
CRDT- 2005/10/26 09:00
PHST- 2005/10/26 09:00 [pubmed]
PHST- 2006/04/25 09:00 [medline]
PHST- 2005/10/26 09:00 [entrez]
AID - 10.1002/jcp.20520 [doi]
PST - ppublish
SO  - J Cell Physiol. 2006 Mar;206(3):709-17. doi: 10.1002/jcp.20520.