IBYME   02675
INSTITUTO DE BIOLOGIA Y MEDICINA EXPERIMENTAL
Unidad Ejecutora - UE
artículos
Título:
INVOLVEMENT OF KLF14 AND EGR-1 IN THE TGF-BETA1 ACTION ON LEYDIG CELL PROLIFERATION
Autor/es:
GONZALEZ C.R.; VALLCANERAS S.S ; CALANDRA R.S, ; GONZALEZ CALVAR S.I.
Revista:
CYTOKINE.
Editorial:
ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD
Referencias:
Lugar: Amsterdam; Año: 2013 p. 670 - 675
ISSN:
1043-4666
Resumen:
Transforming growth factor b1 (TGF-b1) is a pleiotropic cytokine that modulates cell homeostasis. In Leydig
cells, TGF-b1 exerts stimulatory and inhibitory effect depending on the type I receptor involved in the
signaling pathway. The aim of the present work was to study the signaling mechanisms and the intermediates
involved in the action of TGF-b1 on TM3 Leydig cell proliferation in the presence or absence of progesterone.
The MTT assay showed that the presence of progesterone in the culture media lead to a proliferative
effect that was blocked by Ru 486, an inhibitor of progesterone receptor; and ALK-5 did not participate
in this effect.
TGF-b1 (1 ng/ml) increased the expression of p15 (an inhibitor of cell cycle) in TM3 Leydig cells, and
this effect was blocked by progesterone (1 lM). The expression of PCNA presented a higher increase in
the cell cultured with TGF-b1 plus progesterone than in cells cultured only with TGF-b1.
Progesterone induced the gene expression of endoglin, a cofactor of TGF-b1 receptor that leads to a
stimulatory signaling pathway, despite of the absence of progesterone response element in endoglin
gene. In addition, the presence of progesterone induced the gene expression of egr-1 and also KLF14, indicating
that this steroid channels the signaling pathway into a non-canonical mechanism. In conclusion,
these findings suggest that the proliferative action of TGF-b1 involves endoglin. This co-receptor might
be induced by KLF14 which is probably activated by progesterone.