Document Type

Journal Article

Department/Unit

School of Chinese Medicine

Title

ERp57 is up-regulated in free fatty acids-induced steatotic L-02 cells and human nonalcoholic fatty livers

Language

English

Abstract

Pathogenesis of nonalcoholic fatty liver disease (NAFLD) is not clear. In this study we aimed to identify proteins involved in NAFLD development in free fatty acids (FFA)-induced hepatosteatotic cells and in human liver biopsies. Steatosis was induced by incubating a normal human hepatocyte-derived cell line L-02 with FFA. Differentially expressed proteins in the steatotic cells were analyzed by two-dimensional gel electrophoresis-based proteomics. Involvement of one of the up-regulated proteins in steatosis was characterized using the RNA interference approach with the steatotic cells. Protein expression levels in liver biopsies of patients with NAFLD were assessed by immunohistochemistry. Proteomic analysis of L-02 steatotic cells revealed the up-regulation of ERp57, a condition not previously implicated in NAFLD. Knockdown of ERp57 expression with siRNA significantly reduced fat accumulation in the steatotic cells. ERp57 expression was detected in 16 out of 17 patient biopsies and correlated with inflammation grades or fibrosis stages, while in 5 normal biopsies ERp57 expression was not detectable in hepatocytes. In conclusion, ERp57 was up-regulated in FFA-induced steatotic hepatic cells and in NAFLD patient livers and demonstrated steatotic properties in cultured cells. Further investigations are warranted to verify the involvement of ERp57 in NAFLD development. © 2010 Wiley-Liss, Inc.

Keywords

ERp57, L-02 cells, Liver biopsies, Nonalcoholic fatty liver disease, Proteomics

Publication Date

2010

Source Publication Title

Journal of Cellular Biochemistry

Volume

110

Issue

6

Start Page

1447

End Page

1456

Publisher

Wiley

DOI

10.1002/jcb.22696

Link to Publisher's Edition

http://dx.doi.org/10.1002/jcb.22696

ISSN (print)

07302312

ISSN (electronic)

10974644

This document is currently not available here.

Share

COinS