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Titolo:
Developmental exposure to estrogens alters epithelial cell adhesion and gap junction proteins in the adult rat prostate
Autore:
Habermann, H; Chang, WY; Birch, L; Mehta, P; Prins, GS;
Indirizzi:
Univ Illinois, Dept Urol, Chicago, IL 60612 USA Univ Illinois Chicago IL USA 60612 nois, Dept Urol, Chicago, IL 60612 USA Graz Univ, Dept Urol, Graz, Austria Graz Univ Graz AustriaGraz Univ, Dept Urol, Graz, Austria Univ Miami, Sch Med, Dept Med, Miami, FL 33136 USA Univ Miami Miami FL USA 33136 ami, Sch Med, Dept Med, Miami, FL 33136 USA Univ Miami, Sch Med, Sylvester Comprehensive Canc Ctr, Miami, FL 33136 USAUniv Miami Miami FL USA 33136 Comprehensive Canc Ctr, Miami, FL 33136 USA
Titolo Testata:
ENDOCRINOLOGY
fascicolo: 1, volume: 142, anno: 2001,
pagine: 359 - 369
SICI:
0013-7227(200101)142:1<359:DETEAE>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANDROGEN RECEPTOR EXPRESSION; MOLECULE E-CADHERIN; CHICK LIMB BUD; INTERCELLULAR COMMUNICATION; CONNEXIN-43 EXPRESSION; DECREASED EXPRESSION; HIGH-GRADE; CANCER; GENE; LOBES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Prins, GS Univ Illinois, Dept Urol, MC 955, Chicago, IL 60612 USA Univ Illinois MC 955 Chicago IL USA 60612 Chicago, IL 60612 USA
Citazione:
H. Habermann et al., "Developmental exposure to estrogens alters epithelial cell adhesion and gap junction proteins in the adult rat prostate", ENDOCRINOL, 142(1), 2001, pp. 359-369

Abstract

Brief exposure to estrogens during the neonatal period interrupts rat prostatic development by reducing branching morphogenesis and by blocking epithelial cells from entering a normal differentiation pathway. Upon aging, ventral prostates exhibit extensive hyperplasia and dysplasia suggesting that neonatal estrogens may predispose the prostate gland to preneoplastic lesions. To determine whether these prostatic lesions may be manifested through aberrant cell-to-cell communications, the present study examined specific gap junction proteins, Connexins (Cx) 32, and Cx 43, and the cell adhesion molecule, E-cadherin, in the developing, adult and aged rat prostate gland. Male rat pups were given 25 mug estradiol benzoate or oil on days 1, 3, and5 of life. Prostates were removed on days 1, 4, 5, 6, 10, 15, 30, or 90 orat 16 months, and frozen sections were immunostained for E-cadherin, Cx 43, and Cx 32. Colocalization studies were performed with immunofluorescence using specific antibodies for cell markers. Gap junctions in undifferentiated epithelial cells at days 1-10 of life were composed of Cx 43, which always colocalized with basal cell cytokeratins (CK 5/15). Cx 32 expression wasfirst observed between days 10-15 and colocalized to differentiated luminal cells (CK 8/18). Cg 43 and Cx 32 never colocalized to the same cell indicating that junction intercellular communication differs between basal and luminal prostatic cells. While epithelial connexin expression was not initially altered in the developing prostates following estrogen exposure, adult prostates of neonatally estrogenized rats exhibited a marked decrease in Cx32 staining and an increased proportion of Cx 43 expressing cells. In the developing prostate, E-cadherin was localized to lateral surfaces of undifferentiated epithelial cells and staining intensity increased as the cells differentiated into luminal cells. By day 30, estrogenized prostates had small foci of epithelial cells that did not immunostain for E-cadherins. In the adult and aged prostates of estrogenized rats, larger foci with differentiation defects and dysplasia were associated with a decrease or loss in E-cadherin staining. The present findings suggest that estrogen-induced changes in the expression of E-cadherin, Cx32 and Cx43 may result in impaired cell-cell adhesion and defective cell-cell communication and may be one of thekey mechanisms through which changes toward a dysplastic state are mediated. These findings are significant in light of the data on human prostate cancers where carcinogenesis and progression are associated with loss of E-cadherin and a switch from Cx32 to Cx43 expression in the epithelium.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/06/20 alle ore 23:14:23