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Institute of Molecular and Cell Biology (S.M., K.G.), 117609 Singapore; Centre National de la Recherche Scientifique, Unité Mixte de Recherche 5123, Physiologie Moléculaire (M.R., S.B.-B., H.C.M.), 696222 Villeurbanne Cedex, France; and Liggins Institute (D.X.L., P.E.L.), University of Auckland, Private Bag 92019, Auckland, New Zealand
Address all correspondence and requests for reprints to: Peter E. Lobie, M.D. Ph.D., Liggins Institute, University of Auckland, 26 Park Avenue, Private Bag 92019, Auckland, New Zealand. E-mail: p.lobie{at}auckland.ac.nz.
We have examined the expression, postnatal ontogeny, and localization of mouse GH (mGH) and its relative expression during pregnancy, lactation, and weaning in the mouse. mGH mRNA and protein was expressed predominantly in the epithelial component of the mammary gland, and maximal expression was observed during the pubertal period. Autocrine mGH expression dramatically decreased during late pregnancy and lactation. Concordantly, autocrine mGH expression is repressed during forced differentiation of mouse HC11 mammary epithelial cells in culture. Forced expression of mGH in HC11 cells abrogated lactogenic differentiation as indicated by reduced expression of ß-casein and reduced expression and loss of lateral epithelial localization of E-cadherin. Forced expression of mGH in mouse mammary epithelial cells increased cell survival and proliferation and consequently increased the size of mammary acinar-like structures formed in three-dimensional Matrigel. Thus, autocrine mGH expression in the mouse mammary epithelial cell is maximal at puberty and prevents mammary epithelial cell differentiation. Autocrine GH will therefore participate in mammary morphogenic processes at puberty.
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M. J. van den Eijnden and G. J. Strous Autocrine Growth Hormone: Effects on Growth Hormone Receptor Trafficking and Signaling Mol. Endocrinol., November 1, 2007; 21(11): 2832 - 2846. [Abstract] [Full Text] [PDF] |
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