Unlike portal vein, the tunica media cells

of the hepatic artery branches which were appeared during the remodelling stage, were early completely differentiated into smooth muscle cells, selleck screening library expressing regularly ASMA as well as h-caldesmon. These smooth muscle cells of the tunica media might take origin from the tunica media cells of the upstream arteries. However, we cannot exclude that they differentiate from the portal myofibroblasts. IDS2, MKS and ARPKD are autosomal recessively inherited disorders characterised in the liver by abnormal development of the portal tract and notably ductal plate malformation [14–16]. In these diseases, the portal tract stroma is enlarged by fibrosis and contained more stromal cells. As described previously in one case of MKS [17], we showed that, in all our pathological cases, a myofibroblastic subpopulation, which expressed only ASMA persists during HMPL-504 chemical structure all the abnormal maturation of the portal tract and is condensed around the abnormal biliary structures. These myofibroblasts which were present in all portal tracts whatever the calibre of bile ducts and not only in the larger-calibre septal bile ducts, as seen in the normal liver until 2 years of age [12], were probably this website responsible of the excessive deposition of portal extracellular matrix. This myofibroblastic reaction resembles that seen in human liver diseases

affecting bile ducts or in experimental models such as bile duct ligation. However, in these cases, myofibroblasts surrounding the ductular proliferation seemed to derive from the transdifferentiation of portal fibroblasts [23–26]. In the lobular area, the development was the same in all our normal and pathological cases. We showed that HSC are present early in the Disse space and express CRBP-1. The CRBP-1 staining showed that the thin cytoplasmic processes are poorly developed in the beginning and become

more important later. CRBP-1 expressing HSC play a pivotal role in intrahepatic uptake, storage and release of retinoids [27]. As previously described, our study in fetal liver showed that the number of CRBP-1 expressing HSC was variable but gradually increased with the age of development [9, 28]. As shown here, CRBP-1 was also expressed all along the biliary tree from canaliculi to extrahepatic Progesterone bile duct; and this expression was reinforced on the apical/luminale membrane. The bile acid synthesis begins at about 5–9 WD and its secretion at about 12 WD. Bile contains retinoids [29]. We assume that, besides the blood retinol transport, there is a biliary transport of retinoids [3]. Conclusion Our study shows that, during the portal tract development, the portal mesenchymal cells are involved in a morphological phenotypic shift from myofibroblasts to portal fibroblasts and vascular smooth muscle cells; in case of portal fibrosis following ductal plate malformation, portal myofibroblasts persist around the abnormal biliary structures.