Evidence for a role of TGF-beta1 in the expression and regulation of alpha-SMA in fetal growth restricted placentae

There is evidence that alpha-smooth muscle actin (alpha-SMA) is a protein that plays a pivotal role in the production of contractile forces and it is induced by transforming growth factor-beta1 (TGF-beta1). We have analysed the expression of alpha-SMA, TGF-beta1, its receptor RI and the activator ph...

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Bibliographic Details
Published in:Placenta (Eastbourne) 2007-11, Vol.28 (11-12), p.1123-1132
Main Authors: Todros, T, Marzioni, D, Lorenzi, T, Piccoli, E, Capparuccia, L, Perugini, V, Cardaropoli, S, Romagnoli, R, Gesuita, R, Rolfo, A, Paulesu, L, Castellucci, M
Format: Article
Language:English
Subjects:
Actins - metabolism
Adult
Female
Fetal Growth Retardation - physiopathology
Fetus
Gene Expression Regulation
Humans
Placenta - blood supply
Placenta - physiopathology
Pre-Eclampsia - physiopathology
Pregnancy
Pregnancy Complications
Protein-Serine-Threonine Kinases - genetics
Protein-Serine-Threonine Kinases - metabolism
Receptors, Transforming Growth Factor beta - genetics
Receptors, Transforming Growth Factor beta - metabolism
RNA, Messenger - metabolism
Signal Transduction
Transforming Growth Factor beta1 - genetics
Transforming Growth Factor beta1 - metabolism
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Summary:There is evidence that alpha-smooth muscle actin (alpha-SMA) is a protein that plays a pivotal role in the production of contractile forces and it is induced by transforming growth factor-beta1 (TGF-beta1). We have analysed the expression of alpha-SMA, TGF-beta1, its receptor RI and the activator phospho-Smad2 in (a) fetal growth restriction pre-eclamptic placentae characterised by early onset and absence of end diastolic velocities in the umbilical arteries (FGR-AED) and (b) control placentae accurately matched for gestational age. The study was performed by immunohistochemical, quantitative Western blotting, ELISA, RT-PCR and in vitro analyses. We found that TGF-beta1 stimulates alpha-SMA production in chorionic villi cultured in vitro. In addition, we observed that in vivo TGF-beta1 concentration is significantly higher in FGR-AED placental samples than in control placentae and that this growth factor could have a paracrine action on villous stroma myofibroblasts expressing TGF-beta1 receptors and phospho-Smad2. Indeed, we report that alpha-SMA undergoes a redistribution in FGR-AED placental villous tree, i.e. we show that alpha-SMA is enhanced in medium and small stem villi and significantly decreased in the peripheral villi. Our data allow us to consider TGF-beta1 and alpha-SMA as key molecules related to FGR-AED placental villous tree phenotypic changes responsible for increased impedance to blood flow observable in this pathology.
ISSN:0143-4004