Title

Mullerian-inhibiting substance type II receptor expression and function in purified rat Leydig cells

UMMS Affiliation

Department of Pediatrics

Date

6-1-1999

Document Type

Article

Medical Subject Headings

Animals; Anti-Mullerian Hormone; Cells, Cultured; DNA; *Glycoproteins; Growth Inhibitors; Leydig Cells; Male; RNA, Messenger; Rats; Rats, Sprague-Dawley; Receptors, Peptide; Receptors, Transforming Growth Factor beta; Testicular Hormones

Disciplines

Cell Biology | Developmental Biology | Endocrinology

Abstract

Mullerian-inhibiting substance (MIS), a gonadal hormone in the transforming growth factor-beta superfamily, induces Mullerian 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 Mullerian 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.

Rights and Permissions

Citation: Endocrinology. 1999 Jun;140(6):2819-27. Link to article on publisher's site

Comments

At the time of publication, Mary Lee was not yet affiliated with the University of Massachusetts Medical School.

Related Resources

Link to Article in PubMed

PubMed ID

10342873