ANALYSIS OF MULTIPLE GAP JUNCTION GENE-PRODUCTS IN THE RODENT AND HUMAN MAMMARY-GLAND

Citation
A. Pozzi et al., ANALYSIS OF MULTIPLE GAP JUNCTION GENE-PRODUCTS IN THE RODENT AND HUMAN MAMMARY-GLAND, Experimental cell research, 220(1), 1995, pp. 212-219
Citations number
42
Categorie Soggetti
Oncology,"Cell Biology
Journal title
ISSN journal
00144827
Volume
220
Issue
1
Year of publication
1995
Pages
212 - 219
Database
ISI
SICI code
0014-4827(1995)220:1<212:AOMGJG>2.0.ZU;2-Q
Abstract
The expression and localization of three different connexins (alpha 1, Cx43; beta(1), Cx32; and beta(2), Cx26) were analyzed in human, mouse , and rat mammary glands by PCR analysis of reverse-transcribed RNA (R T-PCR) and indirect immunohistochemistry. For the rodent mammary gland , the study included different physiological stages of development dur ing nonpregnancy, pregnancy, lactation, and postweaning. RT-PCR amplif ication revealed a constitutive expression of RNA for alpha(1) connexi n in all three species. In contrast, both beta(1) and beta(2) transcri pts were expressed only during lactation in the rodent mammary gland. Specifically, immunohistochemistry showed that the expression of all t hree connexins was restricted to specific cell types, and it varied ac cording to the physiological activity of the organ. In particular, alp ha(1) antigen was detected only between myoepithelial cells, the contr actile cells surrounding alveoli and ductal systems in the mammary gla nd, while beta(1) and beta(2) antigens were localized solely at the ba solateral border of alveolar secretory cells. The level of beta(1) and beta(2) connexins was increased in the rodent mammary gland during la ctation. No staining for either beta connexin was detected in human ma mmary gland or in that of nonpregnant, pregnant, or postweaning rodent s. The inducible coexpression of beta(1) and beta(2) antigens in lumin al cells of the lactating rodent suggests a possible role for these co nnexins in the coordination of the secretory epithelium. (C) 1996 Acad emic Press, Inc.