Abstract:
:Benign prostatic hyperplasia is a nonmalignant enlargement of the prostate that commonly occurs in older men. We show that liver X receptor (Lxr)-α knockout mice (lxrα(-/-)) develop ventral prostate hypertrophy, correlating with an overaccumulation of secreted proteins in prostatic ducts and an alteration of vesicular trafficking in epithelial cells. In the fluid of the lxrα(-/-) prostates, spermine binding protein is highly accumulated and shows a 3000-fold increase of its mRNA. This overexpression is mediated by androgen hypersensitivity in lxrα(-/-) mice, restricted to the ventral prostate. Generation of chimeric recombinant prostates demonstrates that Lxrα is involved in the establishment of the epithelial-mesenchymal interactions in the mouse prostate. Altogether these results point out the crucial role of Lxrα in the homeostasis of the ventral prostate and suggest lxrα(-/-) mice may be a good model to investigate the molecular mechanisms of benign prostatic hyperplasia.
journal_name
Endocrinologyjournal_title
Endocrinologyauthors
Viennois E,Esposito T,Dufour J,Pommier A,Fabre S,Kemeny JL,Guy L,Morel L,Lobaccaro JM,Baron Sdoi
10.1210/en.2011-1996subject
Has Abstractpub_date
2012-07-01 00:00:00pages
3211-23issue
7eissn
0013-7227issn
1945-7170pii
en.2011-1996journal_volume
153pub_type
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