Expression of the aryl hydrocarbon receptor (AhR) and the aryl hydrocarbon receptor nuclear translocator (ARNT) in fetal, benign hyperplastic, and malignant prostate

被引:0
作者
Kashani, M
Steiner, G
Haitel, A
Schaufler, K
Thalhammer, T
Amann, G
Kramer, G
Marberger, M
Schöller, A
机构
[1] Univ Vienna, Dept Urol, A-1090 Vienna, Austria
[2] Univ Vienna, Dept Clin Pathol, A-1090 Vienna, Austria
[3] Univ Vienna, Dept Gen & Expt Pathol, A-1090 Vienna, Austria
关键词
aryl hydrocarbon receptor; prostatic neoplasms; prostatic hypertrophy;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BACKGROUND. Androgen-dependent tissue has been reported to be affected by chemical ligands of the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, which heterodimerizes with the aryl hydrocarbon receptor nuclear translocator protein (ARNT). METHODS. Fetal (n = 3), benign hyperplastic (BPH) (n = 10), and carcinomatous (CaP) (n = 19) prostate tissues were analyzed using immunohistochemistry. Western blot analysis was used to confirm the identity of the recognized proteins. RESULTS. Immunoblotting of enriched prostatic epithelial cells (EC) and stromal cells revealed constitutive expression of bands at around 110 kDa and 90 kDa, using anti-AhR and anti-ARNT, respectively. Immunohistology of the fetal specimens revealed heterogeneous cytoplasmic and nuclear AhR expression of immature EC and mesenchymal cells. Constitutive expression of AhR (primarily cytoplasmic) and ARNT (nuclear and cytoplasmic) by the majority of adult basal and secretory EC, CaP, and smooth muscle cells was confirmed in situ. The most intense anti-AhR/-ARNT reactivity was found on smooth muscle cells, followed by EC and fibrocytes. Secretory BPH-EC revealed significantly decreased AhR expression when compared to normal tissue segments. By contrast, anti-AhR reactivity was frequently increased in the more dedifferentiated tumor areas. CONCLUSIONS. These findings suggest that an undefined physiologic AhR ligand(s) as well as environmental factors may exert effects on EC and smooth muscle cells in the prostate through binding to these receptors. (C) 1998 Wiley-Liss, Inc.
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页码:98 / 108
页数:11
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