title: TGF-beta1 system in Leydig cells. Part I: effect of hCG and progesterone.
abstract: Transforming growth factor beta 1 (TGF-beta1) modulates male reproductive function. Genetically modified mice overexpressing alpha/beta 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.
authors.affiliation: Instituto de Biología y Medicina Experimental, Buenos Aires, Argentina.
authors.forename: Candela R
authors.initials: CR
authors.lastname: Gonzalez
authors.forename: Betina
authors.initials: B
authors.lastname: Gonzalez
authors.forename: Susana B
authors.initials: SB
authors.lastname: Rulli
authors.forename: Ilpo
authors.initials: I
authors.lastname: Huhtaniemi
authors.forename: Ricardo S
authors.initials: RS
authors.lastname: Calandra
authors.forename: Silvia I
authors.initials: SI
authors.lastname: Gonzalez-Calvar
mesh_terms: D030201:Activin Receptors, Type I / Q000235:genetics / Q000378:metabolism; D030301:Activin Receptors, Type II; D000367:Age Factors; D000818:Animals; D002478:Cells, Cultured; D006063:Chorionic Gonadotropin / Q000235:genetics / Q000494:pharmacology*; D000071063:Endoglin; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism; D007985:Leydig Cells / Q000187:drug effects* / Q000378:metabolism* / Q000502:physiology; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D011374:Progesterone / Q000494:pharmacology*; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D000077293:Receptor, Transforming Growth Factor-beta Type I; D018125:Receptors, Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism; D012741:Sexual Maturation / Q000235:genetics / Q000502:physiology; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology*
chemical_list: D006063:Chorionic Gonadotropin; D000071063:Endoglin; C502004:Eng protein, mouse; D047908:Intracellular Signaling Peptides and Proteins; D018125:Receptors, Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D011374:Progesterone; D017346:Protein Serine-Threonine Kinases; D030201:Activin Receptors, Type I; D030301:Activin Receptors, Type II; C498931:Acvrl1 protein, mouse; D000077293:Receptor, Transforming Growth Factor-beta Type I; C000625842:Tgfbr1 protein, mouse