| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
The Jackson Laboratory, Bar Harbor, Maine
Immunohistochemical analysis using paraffin-embedded specimens is the method of choice to evaluate protein expression at a cellular level while preserving tissue architecture in normal and neoplastic tissues. Current knowledge of the expression of terminal differentiation markers in the mouse mammary gland relies on the evaluation of frozen tissues by use of immunofluorescence. We assessed changes in patterns of expression of terminal differentiation markers throughout the development of the mouse mammary gland in paraffin-embedded tissues. The expression of 
-smooth muscle actin (SMA) and keratins (K) 5, 8/18, and 14 was influenced by the development stage of the mammary gland. Expression of K5 and SMA was restricted to basal cells. Keratin 14 was consistently expressed by mammary basal cells, and was detected in scattered luminal cells from 13.5 days after conception through puberty. Labeling for K8/18 of luminal cells was heterogeneous at all times. Heterogeneous expression patterns in luminal cells suggest this layer has cells with a variety of biological functions. The absence of K6 expression at any stage of the development of the mammary gland was confirmed by use of reverse transcriptase-polymerase chain reaction analysis, which indicates that this intermediate filament is not a marker of the mammary gland stem cell. Finally, consistent with results of earlier studies, keratins 1, 10, 13, and 15, and filaggrin, involucrin, and loricrin were not detected at any stage of mammary gland development.
Key words: Development; immunohistochemistry; intermediate filament; mammary gland; terminal differentiation marker.
Igor Mikaelian, Box #98, The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609-1500 (USA). E-mail: imikaeli{at}jax.org
This article has been cited by other articles:
 |
|
 |
|
  C. Jacob, H. Grabner, S. Atanasoski, and U. Suter Expression and localization of Ski determine cell type-specific TGF{beta} signaling effects on the cell cycle J. Cell Biol., August 11, 2008; 182(3): 519 - 530. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Bierie, D. G. Stover, T. W. Abel, A. Chytil, A. E. Gorska, M. Aakre, E. Forrester, L. Yang, K.-U. Wagner, and H. L. Moses Transforming Growth Factor-{beta} Regulates Mammary Carcinoma Cell Survival and Interaction with the Adjacent Microenvironment Cancer Res., March 15, 2008; 68(6): 1809 - 1819. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Rossiter, C. Barresi, M. Ghannadan, F. Gruber, M. Mildner, D. Fodinger, and E. Tschachler Inactivation of VEGF in mammary gland epithelium severely compromises mammary gland development and function FASEB J, December 1, 2007; 21(14): 3994 - 4004. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. E. Wood, J. M. Hester, and J. M. Cline Mammary Gland Development in Early Pubertal Female Macaques Toxicol Pathol, October 1, 2007; 35(6): 793 - 803. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Boyd and A. Naray-Fejes-Toth Steroid-Mediated Regulation of the Epithelial Sodium Channel Subunits in Mammary Epithelial Cells Endocrinology, August 1, 2007; 148(8): 3958 - 3967. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Q. Yang, R. Kurotani, A. Yamada, S. Kimura, and F. J. Gonzalez Peroxisome Proliferator-Activated Receptor {alpha} Activation during Pregnancy Severely Impairs Mammary Lobuloalveolar Development in Mice Endocrinology, October 1, 2006; 147(10): 4772 - 4780. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
