PMID- 10386469
OWN - NLM
STAT- MEDLINE
DCOM- 19990708
LR  - 20190915
IS  - 0270-4137 (Print)
IS  - 0270-4137 (Linking)
VI  - 40
IP  - 2
DP  - 1999 Jul 1
TI  - Fas antigen/CD-95 upregulation and activation during castration-induced
      regression of the rat ventral prostate gland.
PG  - 89-96
AB  - BACKGROUND: Fas antigen/CD 95 is a 45-kDa transmembrane protein that can initiate
      intracellular signaling pathways, leading to apoptosis when it is clustered on
      the cell surface. A recent report claiming that the ventral prostate glands of
      lpr -/- mutant mice (lacking functional fas antigen) do not regress following
      castration prompted our analysis of the regressing rat ventral prostate gland for
      evidence that fas antigen might participate in the molecular process leading to
      prostate cell apoptosis after castration. METHODS: An RNase protection assay and 
      Western blotting analysis were used to quantify fas antigen mRNA and protein
      expression in the regressing rat ventral prostate gland. Immunoprecipitates of
      fas antigen from membrane preparations made from control or castrated rat
      prostates were analyzed for coprecipitation of FADD and RIP proteins to assess
      the activation state of the fas antigen before and after castration. Finally,
      prostate tissues obtained from two different strains of lpr -/- mutant mice were 
      analyzed for induced apoptosis after castration by the TUNEL staining method.
      RESULTS: Rat ventral prostate gland fas antigen mRNA and protein expression was
      upregulated approximately 3-5-fold in the 3-day castrated rat as compared to
      hormonally intact rats. Immunoprecipitates of fas antigen from membranes of
      ventral prostates from castrated rats contained significantly increased amounts
      of both FADD and RIP proteins when compared to those of intact or control
      operated rats. However, counts of TUNEL-labeled cells in the ventral prostate
      glands of castrated lpr -/- mice were not significantly different from those in
      castrated, genetically normal controls. Likewise, the morphology of apoptotic
      bodies formed in the prostates of castrated lpr -/- mice was indistinguishable
      from that in control animals. CONCLUSIONS: Fas antigen/CD-95, a protein that is
      involved in some forms of apoptosis, is upregulated during regression of the rat 
      ventral prostate gland and becomes functionally "activated." However, our
      inability to distinguish any difference in the apoptosis rate or in the
      morphology of the apoptotic bodies formed in response to castration between lpr
      -/- mice and genetically normal controls indicates that, contrary to the prior
      report, functional fas protein is not required for castration-induced prostate
      cell apoptosis.
FAU - de la Taille, A
AU  - de la Taille A
AD  - Department of Urology, College of Physicians and Surgeons of Columbia University,
      New York, New York 10032, USA.
FAU - Chen, M W
AU  - Chen MW
FAU - Shabsigh, A
AU  - Shabsigh A
FAU - Bagiella, E
AU  - Bagiella E
FAU - Kiss, A
AU  - Kiss A
FAU - Buttyan, R
AU  - Buttyan R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Prostate
JT  - The Prostate
JID - 8101368
RN  - 0 (RNA, Messenger)
RN  - 0 (fas Receptor)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - Cell Membrane/chemistry
MH  - *Gene Expression Regulation
MH  - Immunosorbent Techniques
MH  - In Situ Nick-End Labeling
MH  - Kinetics
MH  - Male
MH  - Mice
MH  - Mice, Inbred C3H
MH  - Mice, Knockout
MH  - *Orchiectomy
MH  - Prostate/chemistry/*cytology/*metabolism
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - fas Receptor/analysis/*genetics
EDAT- 1999/07/01 10:00
MHDA- 2000/06/20 09:00
CRDT- 1999/07/01 10:00
PHST- 1999/07/01 10:00 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1999/07/01 10:00 [entrez]
AID - 10.1002/(SICI)1097-0045(19990701)40:2<89::AID-PROS4>3.0.CO;2-E [pii]
AID - 10.1002/(sici)1097-0045(19990701)40:2<89::aid-pros4>3.0.co;2-e [doi]
PST - ppublish
SO  - Prostate. 1999 Jul 1;40(2):89-96. doi:
      10.1002/(sici)1097-0045(19990701)40:2<89::aid-pros4>3.0.co;2-e.