TGF-beta1 system in Leydig cells. Part I: Effect of hCG and progesterone.

GONZALEZ, C; GONZALEZ B; RULLI S; HUHTANIEMI I; CALANDRA RS; GONZALEZ-CALVAR, SI

JOURNAL OF REPRODUCTION AND DEVELOPMENT

JAPANESE SOC ANIMAL REPRODUCTION, C/O I P E C, INC

Lugar: Japón; Año: 2010 vol. 56 p. 389 - 395

0916-8818

Transforming growth factor beta 1 (TGF-beta1) modulates male reproductive function. Genetically modified mice overexpressing a/b subunits of hCG (hCG+) show Leydig cell hyperplasia/hypertrophy at prepuberty that disappears as the mice approach adulthood. In this study we analyzed the gene expression of TGF-beta1, its specific receptors, type II (TGF-betaRII) and type I (activin receptor-like kinase 1 and 5: ALK1 and ALK5), and co-receptor endoglin (CD105) in purified Leydig cells from hCG+ and wild-type mice at 3 and 8 weeks of age and the occurrence of TGF-beta1, ALK1 and ALK5 by immunohistochemistry. The expression of TGF-beta1 was higher in hCG+ mice at both ages studied, and no changes were observed in TGF-betaRII. ALK5 diminished with age in wild-type mice, whereas ALK1 decreased in hCG+ mice at 8 weeks of age. Endoglin expression showed a marked increase in 3-week-old hCG+ animals. In vitro incubation of Leydig cells from wild-type animals with hCG (10 IU/ml) increased TGF-beta1 and ALK5 expression. Progesterone (10-6 M) induced endoglin expression. These studies provide novel evidence for differential gene and protein expression of ALK1 and ALK5 at different ages and endoglin expression and hormonal, in purified Leydig cells.