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Endocrinology Program, Biomedical Division of the Center of Alcohol Studies and Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, New Jersey 08901
Address all correspondence and requests for reprints to: Dr. Dipak K. Sarkar, Endocrinology Program, Rutgers, The State University of New Jersey, 84 Lipman Drive, New Brunswick, New Jersey 08901. E-mail: sarkar{at}aesop.rutgers.edu.
Estradiol is known to increase lactotropic cell proliferation, but estradiol susceptibility varies among human populations and among various strains of rats. We had reported that folliculostellate (FS) cells regulate estradiols mitogenic action on lactotropes; therefore, we studied their role in determining the susceptibility to estradiol in a high estradiol-responsive rat strain, Fischer 344 (F344), and in a low-responsive strain, Sprague Dawley (SD). Determination of total S-100-positive FS cells in the pituitary revealed that F344 rats have significantly more FS cells than do SD rats. Estradiol treatment did not change the number of FS cells in both F344 and SD rats. When cotransplanted with F344 pituitaries under the kidney capsule or cocultured with F344-derived lactotropes in vitro, FS cells derived from F344 rats increased estradiols mitogenic action. They also increased estradiols mitogenic action on SD-derived lactotropes in primary cultures. However, SD-derived FS cells failed to increase estrogens action on F344- or SD-derived lactotropes. The levels of basic fibroblast growth factor production and secretion by TGF-ß3 and estradiol were much higher in F344-derived FS cells than in SD-derived FS cells. However, the lactotropes growth response to basic fibroblast growth factor was similar in both strains. These data suggest that cell-cell interaction between FS cells and lactotropes regulates estradiols mitogenic action on lactotropes and also determines lactotrope susceptibility to the steroid.
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