Down-regulation of negative acute-phase response genes by hypotonic stress in HepG2 hepatoma cells

Sophie Claeyssens, Fatima Banine, Philippe Rouet, Alain Lavoinne, Jean Philippe Salier

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

An increased hepatocellular hydration state (HS) that can be induced by hypotonic stress or a high glutamine uptake modulates the transcription of given genes in liver. This could be important in the acute phase (AP) of a systemic inflammation where both HS and glutamine uptake transiently increase in liver. In HepG2 hepatoma cells cultured in conditions of hypotonic stress or a high extracellular glutamine availability, a specifically decreased expression of two human mRNAs, namely those of α1-microglobulin/bikunin precursor (AMBP) and α2-HS-glycoprotein, that are also down-regulated in liver by AP, could be seen. A functional analysis of the AMBP promoter indicated that this hypotonic stress-induced down-regulation takes place at a transcriptional level. In these experiments, the mRNA level and transcription of the glyceraldehyde-3-phosphate dehydrogenase gene that are known to be unmodified in AP did not exhibit any change. Given that hypotonic stress also up-regulates the transcription of a liver gene that is also up-regulated in AP [Meisse et al. (1998) FEBS Lett. 422, 346-348], the AP-associated increase in hepatocellular HS now appears to participate in the transcriptional control of both sets of genes that are up- or down-regulated in AP. Copyright (C) 1998 Federation of European Biochemical Societies.

Original languageEnglish (US)
Pages (from-to)15-18
Number of pages4
JournalFEBS Letters
Volume433
Issue number1-2
DOIs
StatePublished - Aug 14 1998
Externally publishedYes

Fingerprint

Acute-Phase Reaction
Osmotic Pressure
Hep G2 Cells
Hydration
Liver
Hepatocellular Carcinoma
Transcription
Down-Regulation
Genes
Glutamine
Functional analysis
Messenger RNA
Glyceraldehyde-3-Phosphate Dehydrogenases
Glycoproteins
Up-Regulation
Availability
Inflammation
Experiments

Keywords

  • Acute-phase gene
  • Glutamine
  • Hepatoma cell
  • Hydration state
  • Transcriptional regulation

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Down-regulation of negative acute-phase response genes by hypotonic stress in HepG2 hepatoma cells. / Claeyssens, Sophie; Banine, Fatima; Rouet, Philippe; Lavoinne, Alain; Salier, Jean Philippe.

In: FEBS Letters, Vol. 433, No. 1-2, 14.08.1998, p. 15-18.

Research output: Contribution to journalArticle

Claeyssens, Sophie ; Banine, Fatima ; Rouet, Philippe ; Lavoinne, Alain ; Salier, Jean Philippe. / Down-regulation of negative acute-phase response genes by hypotonic stress in HepG2 hepatoma cells. In: FEBS Letters. 1998 ; Vol. 433, No. 1-2. pp. 15-18.
@article{5c3d237a138746ac8d818707b870c2d5,
title = "Down-regulation of negative acute-phase response genes by hypotonic stress in HepG2 hepatoma cells",
abstract = "An increased hepatocellular hydration state (HS) that can be induced by hypotonic stress or a high glutamine uptake modulates the transcription of given genes in liver. This could be important in the acute phase (AP) of a systemic inflammation where both HS and glutamine uptake transiently increase in liver. In HepG2 hepatoma cells cultured in conditions of hypotonic stress or a high extracellular glutamine availability, a specifically decreased expression of two human mRNAs, namely those of α1-microglobulin/bikunin precursor (AMBP) and α2-HS-glycoprotein, that are also down-regulated in liver by AP, could be seen. A functional analysis of the AMBP promoter indicated that this hypotonic stress-induced down-regulation takes place at a transcriptional level. In these experiments, the mRNA level and transcription of the glyceraldehyde-3-phosphate dehydrogenase gene that are known to be unmodified in AP did not exhibit any change. Given that hypotonic stress also up-regulates the transcription of a liver gene that is also up-regulated in AP [Meisse et al. (1998) FEBS Lett. 422, 346-348], the AP-associated increase in hepatocellular HS now appears to participate in the transcriptional control of both sets of genes that are up- or down-regulated in AP. Copyright (C) 1998 Federation of European Biochemical Societies.",
keywords = "Acute-phase gene, Glutamine, Hepatoma cell, Hydration state, Transcriptional regulation",
author = "Sophie Claeyssens and Fatima Banine and Philippe Rouet and Alain Lavoinne and Salier, {Jean Philippe}",
year = "1998",
month = "8",
day = "14",
doi = "10.1016/S0014-5793(98)00868-0",
language = "English (US)",
volume = "433",
pages = "15--18",
journal = "FEBS Letters",
issn = "0014-5793",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - Down-regulation of negative acute-phase response genes by hypotonic stress in HepG2 hepatoma cells

AU - Claeyssens, Sophie

AU - Banine, Fatima

AU - Rouet, Philippe

AU - Lavoinne, Alain

AU - Salier, Jean Philippe

PY - 1998/8/14

Y1 - 1998/8/14

N2 - An increased hepatocellular hydration state (HS) that can be induced by hypotonic stress or a high glutamine uptake modulates the transcription of given genes in liver. This could be important in the acute phase (AP) of a systemic inflammation where both HS and glutamine uptake transiently increase in liver. In HepG2 hepatoma cells cultured in conditions of hypotonic stress or a high extracellular glutamine availability, a specifically decreased expression of two human mRNAs, namely those of α1-microglobulin/bikunin precursor (AMBP) and α2-HS-glycoprotein, that are also down-regulated in liver by AP, could be seen. A functional analysis of the AMBP promoter indicated that this hypotonic stress-induced down-regulation takes place at a transcriptional level. In these experiments, the mRNA level and transcription of the glyceraldehyde-3-phosphate dehydrogenase gene that are known to be unmodified in AP did not exhibit any change. Given that hypotonic stress also up-regulates the transcription of a liver gene that is also up-regulated in AP [Meisse et al. (1998) FEBS Lett. 422, 346-348], the AP-associated increase in hepatocellular HS now appears to participate in the transcriptional control of both sets of genes that are up- or down-regulated in AP. Copyright (C) 1998 Federation of European Biochemical Societies.

AB - An increased hepatocellular hydration state (HS) that can be induced by hypotonic stress or a high glutamine uptake modulates the transcription of given genes in liver. This could be important in the acute phase (AP) of a systemic inflammation where both HS and glutamine uptake transiently increase in liver. In HepG2 hepatoma cells cultured in conditions of hypotonic stress or a high extracellular glutamine availability, a specifically decreased expression of two human mRNAs, namely those of α1-microglobulin/bikunin precursor (AMBP) and α2-HS-glycoprotein, that are also down-regulated in liver by AP, could be seen. A functional analysis of the AMBP promoter indicated that this hypotonic stress-induced down-regulation takes place at a transcriptional level. In these experiments, the mRNA level and transcription of the glyceraldehyde-3-phosphate dehydrogenase gene that are known to be unmodified in AP did not exhibit any change. Given that hypotonic stress also up-regulates the transcription of a liver gene that is also up-regulated in AP [Meisse et al. (1998) FEBS Lett. 422, 346-348], the AP-associated increase in hepatocellular HS now appears to participate in the transcriptional control of both sets of genes that are up- or down-regulated in AP. Copyright (C) 1998 Federation of European Biochemical Societies.

KW - Acute-phase gene

KW - Glutamine

KW - Hepatoma cell

KW - Hydration state

KW - Transcriptional regulation

UR - http://www.scopus.com/inward/record.url?scp=0031864450&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031864450&partnerID=8YFLogxK

U2 - 10.1016/S0014-5793(98)00868-0

DO - 10.1016/S0014-5793(98)00868-0

M3 - Article

C2 - 9738923

AN - SCOPUS:0031864450

VL - 433

SP - 15

EP - 18

JO - FEBS Letters

JF - FEBS Letters

SN - 0014-5793

IS - 1-2

ER -