@entity1575 is produced by myofibroblasts of different origins. In culture models, @entity35 myofibroblasts derived from hepatic stellate cells (HSCs) and from periductal portal mesenchymal cells, show distinct proliferative and immunophenotypic evolutive profiles, in particular regarding @entity10944 microfilament (overexpressed vs shut-down, respectively). Here, we examined the contributions of both cell types, in two @entity35 models of @entity1448 , arterial @entity409 and bile duct ligation (BDL). Serum and (immuno)histochemical hepatic analyses were performed at different time points (2 days, 1, 2 and 6 weeks) after injury induction. @entity99 , as attested by serum biochemical tests, was moderate/resolutive in @entity63 vs severe and sustained in BDL. Spatio-temporal and morphometric analyses of @entity29973 and Sirius red stainings showed that in both models, @entity82 accumulated around reactive bile ductules, with a significant correlation between the progression rates of @entity82 and of the ductular reaction (both higher in BDL). After 6 weeks, @entity82 was stabilized and did not exceed F2 (METAVIR) in @entity63 , whereas micronodular cirrhosis (F4) was established in BDL. Immuno-analyses of @entity1918 and @entity10944 expression profiles showed that intralobular HSCs underwent early phenotypic changes marked by @entity10944 overexpression in both models and that the accumulation of @entity82 coincided with that of alpha-SMA-labeled myofibroblasts around portal/septal ductular structures. With the exception of @entity10944 -positive myofibroblasts located at the portal/septal-lobular interface at early stages, and of myofibroblastic HSCs detected together with fine lobular septa in BDL cirrhotic liver, the vast majority of myofibroblasts were @entity10944 -negative. These findings suggest that both in resolutive and sustained @entity1448 , @entity82 is produced by myofibroblasts that derive predominantly from portal/periportal mesenchymal cells. While HSCs massively undergo phenotypic changes marked by @entity10944 overexpression, a minority fully converts into matrix-producing myofibroblasts, at sites, which however may be important in the healing process that circumscribes wounded hepatocytes.

Prominent contribution of portal mesenchymal cells to liver XXXX in @entity63 and obstructive @entity1448 .

@entity29973 :: ('360626(Tax:10116)', 'Gene') :: ['cytokeratin-19'] @entity82 :: ('MESH:D005355', 'Disease') :: ['fibrosis'] @entity35 :: ('10116', 'Species') :: ['rat'] @entity63 :: ('MESH:D007511', 'Disease') :: ['arterial ischemia', 'ischemia'] @entity409 :: ('MESH:D008107', 'Disease') :: ['liver ischemia'] @entity1918 :: ('25365(Tax:10116)', 'Gene') :: ['alpha-smooth muscle actin'] @entity10944 :: ('64362(Tax:10116)', 'Gene') :: ['desmin'] @entity1448 :: ('MESH:D002779', 'Disease') :: ['cholestatic injury'] @entity1575 :: ('MESH:D008103', 'Disease') :: ['Liver fibrosis'] @entity99 :: ('MESH:D056486', 'Disease') :: ['Cholestatic liver injury']
@entity82 :: (MESH:D005355,Disease) :: ['fibrosis']
