Immunohistochemical study of the phenotypic change of the mesenchymal cells during portal tract maturation in normal and fibrous (ductal plate malformation) fetal liver

doi:10.1186/1476-5926-8-5

Comparative Hepatology

Volume 8

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Villeneuve J
Pelluard-Nehme F
Combe C
Carles D
Chaponnier C
Ripoche J
Balabaud C
Bioulac-Sage P
Lepreux S

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Villeneuve J
Pelluard-Nehme F
Combe C
Carles D
Chaponnier C
Ripoche J
Balabaud C
Bioulac-Sage P
Lepreux S
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Immunohistochemical study of the phenotypic change of the mesenchymal cells during portal tract maturation in normal and fibrous (ductal plate malformation) fetal liver

Julien Villeneuve¹ , Fanny Pelluard-Nehme² , Chantal Combe¹ , Dominique Carles² , Christine Chaponnier³ , Jean Ripoche¹ , Charles Balabaud¹ , Paulette Bioulac-Sage¹^,2 and Sébastien Lepreux¹^,2

¹INSERM U889, Université Bordeaux2, F-33076 Bordeaux, France

²Service d'Anatomie Pathologique, Hôpital Pellegrin, F-33076 Bordeaux, France

³Département de Pathologie et d'Immunologie, CMU, Genève, Suisse

author email corresponding author email

Comparative Hepatology 2009, 8:5doi:10.1186/1476-5926-8-5


Published:	14 July 2009

Abstract

Background

In adult liver, the mesenchymal cells, portal fibroblasts and vascular smooth muscle cells can transdifferentiate into myofibroblasts, and are involved in portal fibrosis. Differential expression of markers, such as alpha-smooth muscle actin (ASMA), h-caldesmon and cellular retinol-binding protein-1 allows their phenotypic discrimination. The aim of our study was to explore the phenotypic evolution of the mesenchymal cells during fetal development in normal liver and in liver with portal fibrosis secondary to ductal plate malformation in a series of Meckel-Gruber syndrome, autosomal recessive polycystic kidney disease and Ivemark's syndrome.

Results

At the early steps of the portal tract maturation, portal mesenchymal cells expressed only ASMA. During the maturation process, these cells were found condensed around the biliary and vascular structures. At the end of maturation process, only cells around vessels expressed ASMA and cells of the artery tunica media also expressed h-caldesmon. In contrast, ASMA positive cells persisted around the abnormal biliary ducts in fibrous livers.

Conclusion

As in adult liver, there is a phenotypic heterogeneity of the mesenchymal cells during fetal liver development. During portal tract maturation, myofibroblastic cells disappear in normal development but persist in fibrosis following ductal plate malformation.