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Endocrinology Vol. 141, No. 7 2309-2318
Copyright © 2000 by The Endocrine Society

ARTICLES

Role of Estrogen Receptor {alpha} in Hematopoietic Stem Cell Development and B Lymphocyte Maturation in the Male Mouse1

T. Scott Thurmond, Francis G. Murante, J. Erin Staples, Allen E. Silverstone, Kenneth S. Korach and Thomas A. Gasiewicz

Department of Environmental Medicine, University of Rochester (T.S.T., F.G.M., T.A.G.), Rochester, New York 14642; Department of Microbiology and Immunology, State University of New York Health Science Center (J.E.S., A.E.S.), Syracuse, New York 13210; and National Institute of Environmental and Health Sciences (K.S.K.), Research Triangle Park, North Carolina 27709

Address all correspondence and requests for reprints to: Dr. Tom Gasiewicz, Department of Environmental Medicine, University of Rochester, 575 Elmwood Avenue, Box EHSC, Rochester, New York 14642. E-mail: Tom_Gasiewicz{at}urmc.rochester.edu

Although estrogens and estrogen receptors (ERs) are known to function in the male brain and reproductive tract, few studies have evaluated their involvement in the male hematopoietic and immune systems. This study was undertaken to determine the role of ER{alpha} in hematopoietic progenitor and B lymphocyte maturation. ER{alpha} knockout (ER-/-), wild-type (ER+/+), and radiation chimeric (ER{alpha} positive or negative in either nonhematopoietic or hematopoietic elements, or both) male mice were used to determine target tissues. ER-/- and ER+/+ animals showed similar hematopoietic progenitor profiles, but the ER-/- animals had fewer cells in all bone marrow B lymphocyte subpopulations. Animals receiving a pharmacological dose (5 mg/kg BW) of 17ß-estradiol (E2) with both elements, ER+/+, had decreased early hematopoietic progenitors and a shift toward a mature B cell subpopulation, whereas animals with both elements, ER-/-, showed changes only in early hematopoietic progenitors. Hematopoietic element ER+/+ animals exhibited greater E2-induced hematopoietic progenitor and B lymphocyte alterations than those having only nonhematopoietic ER{alpha}. These data indicate that 1) ER{alpha} is not necessary for regulating male mouse normal hematopoietic progenitor cell proportions, but is involved in B cell regulation; and 2) ER{alpha} in hematopoietic elements is predominantly responsible for mediating E2-induced hematopoietic and B cell changes.




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