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World J Gastroenterol. Feb 14, 2014; 20(6): 1554-1564
Published online Feb 14, 2014. doi: 10.3748/wjg.v20.i6.1554
Published online Feb 14, 2014. doi: 10.3748/wjg.v20.i6.1554
Regulation of hepatic EAAT-2 glutamate transporter expression in human liver cholestasis
Mustapha Najimi, Xavier Stéphenne, Etienne Sokal, Université Catholique de Louvain, Institut de Recherche Expérimentale et Clinique (IREC), Laboratory of Pediatric Hepatology and Cell Therapy, Brussels 1200, Belgium
Christine Sempoux, Anatomo-pathology, Cliniques Universitaires St-Luc, Université Catholique de Louvain, Brussels 1200, Belgium
Author contributions: Najimi M performed the majority of experiments; Najimi M designed the study and wrote the manuscript; Stéphenne X participated in performing the in vivo experiments on rats; Stéphenne X, Sempoux C and Sokal E were involved in revising the manuscript; Sempoux C provided the human liver samples, supervised the immunohistochemistry analyses; Sokal E provided the financial support.
Correspondence to: Mustapha Najimi, PhD, Université Catholique de Louvain, Institut de Recherche Expérimentale et Clinique (IREC), Laboratory of Pediatric Hepatology and Cell Therapy, Avenue Mounier 52, Brussels 1200, Belgium. mustapha.najimi@uclouvain.be
Telephone: +32-2-7645283 Fax: +32-2-7645258
Received: April 23, 2013
Revised: September 9, 2013
Accepted: September 16, 2013
Published online: February 14, 2014
Processing time: 299 Days and 18.8 Hours
Revised: September 9, 2013
Accepted: September 16, 2013
Published online: February 14, 2014
Processing time: 299 Days and 18.8 Hours
Core Tip
Core tip: The aim of the current study was to demonstrate the role of glutamate transport, the most abundant intracellular hepatic amino acid, in liver cholestasis. The study was conducted in vitro using HepG2 cells as well as the livers of bile duct ligated rats and human cholestasis specimens. The principal data revealed that the activity and expression of EAAT2-mediated glutamate transport were altered both in vitro and in vivo. This supports the involvement of glutamate transporters, as an indirect liver response and/or as a direct hepatic target, in restoring intracellular pools of this amino acid which are probably altered after cholestasis.