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Journal of Endocrinology (2007) 194, 557-568    DOI: 10.1677/JOE-07-0258
© 2007 Society for Endocrinology
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Inactivation of the IGF-I receptor gene in primary Sertoli cells highlights the autocrine effects of IGF-I

 P Froment1,2,3, M Vigier3, D Nègre4,5,6, I Fontaine7, J Beghelli3, F L Cosset4,5,6, M Holzenberger8 and P Durand1,2,3

1 Institut de Génomique Fonctionnelle de Lyon, Université de Lyon, Lyon F-69003, France
2 INRA, CNRS, Université Lyon 1, Ecole Normale Supérieure, Lyon F-69364, France
3 INSERM U418, Lyon, France
4 Université de Lyon, (UCB-Lyon1), IFR128, Lyon F-69007, France
5 INSERM, U758, Lyon F-69007, France
6 Ecole Normale Supérieure de Lyon, Lyon F-69007, France
7 UMR 6175, INRA, CNRS, Université de Tours, Haras Nationaux, Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France
8 INSERM U515, Hôpital Saint-Antoine, 75571 Paris 12, France

(Requests for offprints should be addressed to P Froment Team Génomique Fonctionnelle de la Reproduction – IGFL, Hôpital Debrousse – 29, rue Soeur Bouvier, 69322 Lyon, France; Email: froment{at}lyon.inserm.fr)

IGF-I regulates pituitaryand gonadal functions, and is pivotal for sexual development and fertility in mammalian species. To better understand the function of autocrine IGF-I in Sertoli cell physiology, we established a system for Cre-mediated conditional inactivation of the IGF-I receptor (IGF-IR) in cultured Sertoli cells. We show here that loss of IGF-IR decreased the number of viable Sertoli cells as a consequence of diminished Sertoli cell proliferation and increased Sertoli cell death. Furthermore, the lack of IGF-IR altered the morphology of cultured Sertoli cells and decreased lactate and transferrin secretions. Collectively, our data indicate that autocrine IGF-I contributes significantly to Sertoli cell homeostasis. The described in vitro system for loss-of-function analysis of the IGF-IR can be readily transposed to study the role of other intratesticular growth factors involved in spermatogenesis.






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Copyright © 2007 by the Society for Endocrinology.