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Endocrinology Vol. 140, No. 6 2819-2827
Copyright © 1999 by The Endocrine Society

ARTICLES

Müllerian-Inhibiting Substance Type II Receptor Expression and Function in Purified Rat Leydig Cells1

Mary M. Lee, Ching Ching Seah2, Peter T. Masiakos, Chantal M. Sottas, Frederic I. Preffer, Patricia K. Donahoe, David T. MacLaughlin and Matthew P. Hardy

The Pediatric Endocrine Unit (M.M.L., C.C.S.), Pediatric Surgical Research Laboratory (P.T.M., P.K.D., D.T.M.) and Department of Pathology (F.I.P.), Massachusetts General Hospital, Boston, Massachusetts 02114; and The Population Council and The Rockefeller University (C.M.S., M.P.H.), New York, New York 10021

Address all correspondence and requests for reprints to: Mary M. Lee, M.D., Pediatric Endocrine Unit, Bartlett Hall Extension 410, 55 Fruit Street, Massachusetts General Hospital, Boston, Massachusetts 02114. E-mail: mlee{at}helix.mgh.harvard.edu

Müllerian-inhibiting substance (MIS), a gonadal hormone in the transforming growth factor-ß superfamily, induces Müllerian duct involution during male sexual differentiation. Mice with null mutations of the MIS ligand or receptor develop Leydig cell hyperplasia and neoplasia in addition to retained Müllerian ducts, whereas MIS-overexpressing transgenic mice have decreased testosterone concentrations and Leydig cell numbers. We hypothesized that MIS directly modulates Leydig cell proliferation and differentiated function in the maturing testis. Therefore, highly purified rat Leydig and Sertoli cells were isolated to examine cell-specific expression, binding, and function of the MIS type II receptor. These studies revealed that this receptor is expressed abundantly in progenitor (21-day) and immature (35-day) Leydig cells as well as in Sertoli cells. Prepubertal progenitor Leydig cells exhibit high affinity (Kd = 15 nM), saturable binding of MIS. No binding, however, is detected with either peripubertal immature Leydig cells or Sertoli cells at either age. Moreover, progenitor, but not immature Leydig cells, respond to MIS by decreasing DNA synthesis. These data demonstrate that functional MIS type II receptors are expressed in progenitor Leydig cells and support the hypothesis that MIS has a direct role in the regulation of postnatal testicular development.




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