Open AccessCharacterization and regulation of somatomedin‐C/insulin‐like growth factor I (Sm‐C/IGF‐I) receptors on cultured pig Leydig cells
Author(s) -
PERRARDSAPORI MarieHélène,
CHATELAIN Pierre G.,
JAILLARD Christine,
SAEZ José M.
Publication year - 1987
Publication title -
european journal of biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1432-1033
pISSN - 0014-2956
DOI - 10.1111/j.1432-1033.1987.tb11213.x
Subject(s) - leydig cell , somatomedin , receptor , endocrinology , medicine , human chorionic gonadotropin , growth factor , insulin like growth factor , dissociation constant , gonadotropin , biology , ed50 , chemistry , hormone , luteinizing hormone
We have characterized somatomedin‐C/insulin‐like growth factor I (Sm‐C/IGF‐I) receptors in cultured pig Leydig cells by binding and cross‐linking affinity experiments. At equilibrium the dissociation constant and the number of binding sites per cell were 1.8 ± 0.2 × 10 −9 M and 12200 ± 3200 respectively. Under reducing conditions, disuccinimidyl suberate cross‐linked 125 I‐Sm‐C to one receptor complex with apparent M r = 120000. Continuous treatment of Leydig cells with increasing concentrations of human chorionic gonadotropin (hCG) for 48 h resulted in a dose‐dependent (ED 50 0.05 nM) increment in IGF type I receptors (2.5–3‐fold increase). Conversely, treatment of Leydig cells for 48 h with increasing concentrations of Sm‐C/IGF‐I produced a 3–4‐fold increase in hCG receptors. This effect was dose‐dependent (ED 50 = 7 ng/ml). Sm‐C/IGF‐I treatment also enhanced Leydig cell responsiveness to hCG for both cAMP (6‐fold) and testosterone (8‐fold). Moreover the stimulatory effects of Sm‐C/IGF‐I on cells cultured either in the absence or presence of 5% human serum from an hypopituitary patient were inhibited by anti‐(Sm‐C/IGF‐I) antibodies. Taken together these results not only show that Leydig cells must be considered as targets for Sm‐C/IGF‐I, but also lend support to the possibility that Sm‐C/IGF‐I plays a role in the regulation of Leydig cell function. Moreover, they suggest that Sm‐C/IGF‐I might be responsible for the delayed puberty observed in some patients with isolated growth hormone deficiency.