Publication: Regulation of human endometrial transforming growth factor ß1 and ß3 isoforms through menstrual cycle and medroxyprogesterone acetate treatment
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Date
2002
Authors
Reis, F.M. ; Ribeiro, M.F.M. ; Maia, A.L. ; Spritzer, P.M.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The progesterone-induced differentiation of
endometrial tissue from proliferative into secretory and
decidua seems to be modulated by locally produced
hormones and cytokines. Transforming growth factor
beta (TGFß), a cytokine produced by endometrial cells,
has been shown to modulate endometrial cell
proliferation in vitro. Our aim was to evaluate the effects
of medroxyprogesterone acetate (MPA) and the
influence of menstrual cycle on the expression of TGFß1
and TGFß3 in human endometrium in vivo. In a doubleblind,
placebo-controlled trial, 46 healthy women with
regular menstrual cycles received either MPA (10
mg/day) or placebo during 10 days. Endometrial and
blood samples were collected 8-12 hours after the last
MPA or placebo administration. Patients were classified
into three groups according to biopsy dating and
treatment: proliferative [tissue]/placebo, secretory
[tissue]/placebo and secretory [tissue]/MPA. The
immunohistochemical distribution of TGFß1 and TGFß1
mRNA was similar in all groups. Immunoreactive
TGFß3 was present in the epithelium in 9.1% of
proliferative samples, in 41.2% of secretory/placebo
samples and in 87.5% of secretory/MPA samples
(p=0.001). In the stroma, the frequency of TGFß3
staining was markedly increased after treatment with
MPA (62.5%) compared to placebo (proliferative: 9.1%;
secretory: 5.9%; p=0.005). The levels of TGFß3 mRNA
increased during the secretory phase and were higher in
the MPA-treated group, being directly correlated with
morphological endometrial differentiation. It is
concluded that MPA administration to healthy women
increased TGFß3 but did not change TGFß1 gene and
protein expression in the endometrium. This finding
suggests that TGFß3 may be a local factor mediating
progesterone- and progestogen-induced endometrial differentiation.
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