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Title: Integrin-linked kinase is involved in matrix-induced hepatocyte differentiation

Abstract

Hepatocytes have restricted proliferative capacity in culture and when cultured without matrix, lose the hepatocyte-specific gene expression and characteristic cellular micro-architecture. Overlay of matrix-preparations on de-differentiated hepatocytes restores differentiation. Integrin-linked kinase (ILK) is a cell-matrix-adhesion protein crucial in fundamental processes such as differentiation and survival. In this study, we investigated the role of ILK, and its binding partners PINCH, {alpha}-parvin, and Mig-2 in matrix-induced hepatocyte differentiation. We report here that ILK is present in the liver and localizes at cell-matrix adhesions of cultured hepatocytes. We also show that ILK, PINCH, {alpha}-parvin, and Mig-2 expression level is dramatically reduced in the re-differentiated hepatocytes. Interestingly, hepatocytes lacking ILK undergo matrix-induced differentiation but their differentiation is incomplete, as judged by monitoring cell morphology and production of albumin. Our results show that ILK and cell-matrix adhesion proteins play an important role in the process of matrix-induced hepatocyte differentiation.

Authors:
 [1];  [1];  [1];  [1];  [1]
  1. Department of Cellular and Molecular Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261 (United States)
Publication Date:
OSTI Identifier:
20979797
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 353; Journal Issue: 3; Other Information: DOI: 10.1016/j.bbrc.2006.12.091; PII: S0006-291X(06)02725-2; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ADHESION; ALBUMINS; GENES; LIVER; LIVER CELLS; MORPHOLOGY

Citation Formats

Gkretsi, Vasiliki, Bowen, William C, Yang, Yu, Wu, Chuanyue, and Michalopoulos, George K. Integrin-linked kinase is involved in matrix-induced hepatocyte differentiation. United States: N. p., 2007. Web. doi:10.1016/j.bbrc.2006.12.091.
Gkretsi, Vasiliki, Bowen, William C, Yang, Yu, Wu, Chuanyue, & Michalopoulos, George K. Integrin-linked kinase is involved in matrix-induced hepatocyte differentiation. United States. doi:10.1016/j.bbrc.2006.12.091.
Gkretsi, Vasiliki, Bowen, William C, Yang, Yu, Wu, Chuanyue, and Michalopoulos, George K. Fri . "Integrin-linked kinase is involved in matrix-induced hepatocyte differentiation". United States. doi:10.1016/j.bbrc.2006.12.091.
@article{osti_20979797,
title = {Integrin-linked kinase is involved in matrix-induced hepatocyte differentiation},
author = {Gkretsi, Vasiliki and Bowen, William C and Yang, Yu and Wu, Chuanyue and Michalopoulos, George K},
abstractNote = {Hepatocytes have restricted proliferative capacity in culture and when cultured without matrix, lose the hepatocyte-specific gene expression and characteristic cellular micro-architecture. Overlay of matrix-preparations on de-differentiated hepatocytes restores differentiation. Integrin-linked kinase (ILK) is a cell-matrix-adhesion protein crucial in fundamental processes such as differentiation and survival. In this study, we investigated the role of ILK, and its binding partners PINCH, {alpha}-parvin, and Mig-2 in matrix-induced hepatocyte differentiation. We report here that ILK is present in the liver and localizes at cell-matrix adhesions of cultured hepatocytes. We also show that ILK, PINCH, {alpha}-parvin, and Mig-2 expression level is dramatically reduced in the re-differentiated hepatocytes. Interestingly, hepatocytes lacking ILK undergo matrix-induced differentiation but their differentiation is incomplete, as judged by monitoring cell morphology and production of albumin. Our results show that ILK and cell-matrix adhesion proteins play an important role in the process of matrix-induced hepatocyte differentiation.},
doi = {10.1016/j.bbrc.2006.12.091},
journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 3,
volume = 353,
place = {United States},
year = {2007},
month = {2}
}