tgfβ1 attenuates expression of prolactin and igfbp-1 in decidualized endometrial stromal cells by both smad-dependent and smad-independent pathwaystgfβ1变弱表达的催乳素和igfbp-1 decidualized smad-dependent和子宫内膜基质细胞smad-independent通路.pdfVIP
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tgfβ1 attenuates expression of prolactin and igfbp-1 in decidualized endometrial stromal cells by both smad-dependent and smad-independent pathwaystgfβ1变弱表达的催乳素和igfbp-1 decidualized smad-dependent和子宫内膜基质细胞smad-independent通路
TGFb1 Attenuates Expression of Prolactin and IGFBP-1 in
Decidualized Endometrial Stromal Cells by Both SMAD-
Dependent and SMAD-Independent Pathways
1¤ 2 2 1 1
Nicole M. Kane , Marius Jones , Jan J. Brosens , Rodney W. Kelly , Philippa T. K. Saunders ,
Hilary O. D. Critchley3*
1 Medical Research Council Human Reproductive Sciences Unit, Centre for Reproductive Biology, Queen’s Medical Research Institute, Edinburgh, Scotland, United
Kingdom, 2 Institute of Reproductive and Developmental Biology, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom, 3 Division of
Reproductive and Developmental Sciences, Centre for Reproductive Biology, Queen’s Medical Research Institute, The University of Edinburgh, Edinburgh, Scotland, United
Kingdom
Abstract
Background: Decidualization (differentiation) of the endometrial stromal cells during the secretory phase of the menstrual
cycle is essential for successful implantation. Transforming Growth Factor b1 (TGFb1) canonically propagates its actions via
SMAD signalling. A role for TGFb1 in decidualization remains to be established and published data concerning effects of
TGF b1 on markers of endometrial decidualization are inconsistent.
Methodology/Principal Findings: Non-pregnant endometrial stromal cells (ESC) and first trimester decidual stromal cells
(DSC) were cultured in the presence or absence of a decidualizing stimulus. Incubation of ESCs with TGFb1 (10 ng/ml)
down-regulated the expression of transcripts encoding the decidual marker proteins prolactin (PRL), insulin-like growth
factor binding protein-1 (IGFBP-1) and tissue factor (TF). TGFb1 also inhibited secretion of PRL and IGFBP-1 proteins by ESCs
and surprisingly this response
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