Cell swelling increased the α2‐macroglobulin gene expression in cultured rat hepatocytes

Meisse, Delphine; Renouf, Sylvie; Husson, Annie; Lavoinne, Alain

doi:10.1016/s0014-5793(98)00038-6

Cited by 12 publications

(14 citation statements)

References 14 publications

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“…Although the transcriptional control of APP genes by pro‐inflammatory cytokines such as tumor necrosis factor (TNF), interleukin‐1 (IL‐1) and IL‐6 is largely proven [12–14], the question now arises as to whether the hepatocellular HS also participates in this control. Indeed, some of us have recently shown that a hypotonic stress‐induced increase in this hepatocellular HS is sufficient to up‐regulate the mRNA level for a positive APP, namely rat α2‐M, via a transcriptional step [6]. We now report for the first time that hypotonic stress, e.g.…”

Section: Introductionmentioning

confidence: 65%

“…This is the first report that hypotonic stress per se is sufficient to down‐regulate the transcription of a negative APP‐encoding gene. Strikingly, this down‐regulation is opposed to the hypotonicity‐driven, transcriptional up‐regulation of a gene encoding a well‐known positive APP, as recently shown with the rat a2‐M gene [6], or that of another gene, namely the rat β‐actin gene [5]whose up‐regulation in endotoxin‐challenged hepatocytes has been observed [32]. Also of great interest is the fact that c‐ jun is another gene whose hepatic mRNA level is up‐regulated by hypotonicity and AP [3, 33].…”

Section: Discussionmentioning

confidence: 83%

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

Claeyssens¹,

Banine²,

Rouet³

et al. 1998

FEBS Letters

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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 K K1-microglobulin/bikunin precursor (AMBP) and K K2-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 upregulates the transcription of a liver gene that is also upregulated 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.z 1998 Federation of European Biochemical Societies.

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Section: Introductionmentioning

confidence: 65%

Section: Discussionmentioning

confidence: 83%

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

Claeyssens¹,

Banine²,

Rouet³

et al. 1998

FEBS Letters

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“…Cytotoxic edema refers to cell swelling that results from intracellular fluid accumulation that occurs during stroke, trauma, or hypoxia (Papadopoulos et al, 2004), and this can be reproduced in vitro by exposing cells to extracellular hypo-osmolarity (Fischer et al, 1997;Caprini et al, 2003). Several genes, including p75NTR, are activated in response to this treatment (Husson et al, 1996;Meisse et al, 1998;Michalke et al, 2000;Warskulat et al, 2001;Peterson and Bogenmann, 2003), but the mechanisms that support this response and its physiological significance remain uncertain. p75NTR is almost invariably expressed after tissue injury that is accompanied by edema, and Peterson and Bogenmann (2003) have proposed that injury-induced reductions in extracellular osmolarity activate p75NTR transcription in vivo.…”

Section: Introductionmentioning

confidence: 99%

Hypo-Osmolar Stress Induces p75NTR Expression by Activating Sp1-Dependent Transcription

Ramos¹,

Ho²,

Forté³

et al. 2007

J. Neurosci.

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Injury-induced expression of the p75 neurotrophin receptor (p75NTR) in the CNS facilitates neuronal apoptosis and prevents neuronal regrowth, but the mechanisms regulating p75NTR expression are poorly characterized. In this study, we showed that hypo-osmolarity induces p75NTR expression in primary neurons, and, using a comparative genomics approach, we identified conserved elements in the 25 kb upstream sequences of the rat, mouse, and human p75NTR genes. We found that only one of these, a proximal region rich in Sp1 sites, responds to changes in hypo-osmolarity. We then showed that Sp1 DNA binding activity is increased in cells exposed to hypoosmolarity, established that hypo-osmolarity enhanced Sp1 binding to the endogenous p75NTR promoter, and showed that Sp1 is required for p75NTR expression induced by hypo-osmolarity. We examined how Sp1 is regulated to effect these changes and established that Sp1 turnover is strongly inhibited by hypo-osmolarity. We propose that stress-induced Sp1 accumulation that results from reductions in Sp1 turnover rate contributes to injury-induced gene expression.

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“…Elle a surtout été étudiée dans les phases aiguës de l'inflammation chez l'animal et peu en situation d'inflammation chronique. Cependant, on sait que sa concentration sérique augmente avec la fibrose [10], une augmentation liée à l'activation des cellules stellaires au cours de la fibrogenèse [11]. L'α2m, inhibe les protéinases et peut donc augmenter la fibrose en inhibant le catabolisme des protéines de la matrice extracellulaire, par exemple en diminuant l'activité des collagénases [12].…”

Section: En Quoi Consistent Les Marqueurs Biochimiques De Fibrose ?unclassified

Biopsie du foie contre prise de sang pour le suivi de l’hépatite C ?

et al. 2002

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353L'évaluation de l'état histologique du foie est considé-rée comme une donnée indispensable pour décider du traitement et du suivi des sujets contaminés par le virus de l'hépatite C (VHC) [1]. La biopsie hépatique n'est toutefois pas un examen anodin [2] et, souvent vécue par les sujets contaminés par le VHC comme un examen agressif [3], elle peut se révéler un obstacle à la prise en charge efficace de l'hépatite C. Une enquête récente (Réseau Hépatite C-Auvergne, chez 1 177 généralistes) a révélé que la biopsie hépatique était refusée par 59 % des patients contaminés par le VHC et que 22 % des médecins interrogés partageaient la même crainte de la biopsie [3]. En dehors de ces enquêtes d'opinion, les études portant sur les complications de la biopsie montrent qu'une douleur est signalée chez un tiers des sujets, qu'une complication sévère existe dans 3 cas sur 1 000 et un décès dans 3 cas sur 10 000 [2,4]. L'utilisation de marqueurs non agressifs de l'état histologique du foie pourrait donc s'avérer très importante pour assurer une prise en charge plus efficace de cette maladie. Dans cet objectif, nous avons mis au point une combinaison de tels marqueurs qui pourrait permettre de diminuer par deux le nombre de biopsies du foie chez les sujets contaminés par le VHC [5].

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Cell swelling increased the α2‐macroglobulin gene expression in cultured rat hepatocytes

Cited by 12 publications

References 14 publications

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

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

Hypo-Osmolar Stress Induces p75NTR Expression by Activating Sp1-Dependent Transcription

Biopsie du foie contre prise de sang pour le suivi de l’hépatite C ?

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