Overexpression of the Complementary DNA for Human Glutamine:Fructose-6-Phosphate Amidotransferase in Mesangial Cells Enhances Glucose-Induced Fibronectin Synthesis and Transcription Factor Cyclic Adenosine Monophosphate-Responsive Element Binding Phosphorylation

Singh, Lalit P.; Alexander, Michelle; Greene, K; Crook, Errol D.

doi:10.1097/00042871-200302000-00025

Cited by 3 publications

(4 citation statements)

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“…Mesangial cells cultured in the presence of high glucose and glucosamine show high levels of O-Nacetylglucosamine in several cytoplasmic and nuclear proteins (Singh et al, 2003). Inhibition of O-glycosylation by benzyl-2-acetamido-2-deoxy-a-D-galactopyranoside blocks both high glucose and glucosamine-induced fibronectin synthesis and CREB phosphorylation.…”

Section: Protein Synthesis and Degradationmentioning

confidence: 99%

“…In addition, mesangial cells exposed to high glucose exhibited an elevated GFAT expression, and became more sensitive to the glucose effects on fibronectin expression and CREB phosphorylation than control cells. The authors then postulated that the hexosamine biosynthesis pathway works as a glucose sensor and mediates at least some of the effects of hyperglycemia in the diabetic kidney (Singh et al, 2003).…”

Section: Protein Synthesis and Degradationmentioning

confidence: 99%

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Molecular mechanisms of glutamine action

Curi

Lagranha

Doi

et al. 2005

Journal Cellular Physiology

416

300

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Glutamine is the most abundant free amino acid in the body and is known to play a regulatory role in several cell specific processes including metabolism (e.g., oxidative fuel, gluconeogenic precursor, and lipogenic precursor), cell integrity (apoptosis, cell proliferation), protein synthesis, and degradation, contractile protein mass, redox potential, respiratory burst, insulin resistance, insulin secretion, and extracellular matrix (ECM) synthesis. Glutamine has been shown to regulate the expression of many genes related to metabolism, signal transduction, cell defense and repair, and to activate intracellular signaling pathways. Thus, the function of glutamine goes beyond that of a simple metabolic fuel or protein precursor as previously assumed. In this review, we have attempted to identify some of the common mechanisms underlying the regulation of glutamine dependent cellular functions.

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Section: Protein Synthesis and Degradationmentioning

confidence: 99%

Section: Protein Synthesis and Degradationmentioning

confidence: 99%

Molecular mechanisms of glutamine action

Curi

Lagranha

Doi

et al. 2005

Journal Cellular Physiology

416

300

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“…5A). We reported that phosphorylated cyclic AMP response element-binding protein (CREB), a major transcriptional co-activator in stress-signaling cascades, is involved in induction of FN expression in mesangial cells (Singh et al, 2003;Singh et al, 2001). Moreover, RAGE (Huttunen et al, 2002;Makam et al, 2009) and p38 MAPK (Ono and Han, 2000) induce CREB phosphorylation.…”

Section: Txnip Mediates Rage-induced Fn and Il-1 Expression In Scsmentioning

confidence: 99%

RAGE–TXNIP axis is required for S100B-promoted Schwann cell migration, fibronectin expression and cytokine secretion

Sbai

Devi

Melone

et al. 2010

Journal of Cell Science

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SummaryDuring peripheral nerve injury, Schwann cells (SCs) adopt a migratory phenotype and remodel the extracellular matrix and provide a supportive activity for neuron regeneration. SCs synthesize neurotrophic factors and cytokines that are crucial for the repair of the injured nerve. The receptor for advanced glycation end products (RAGE) and its ligand S100B, which are secreted by SCs, are required for the repair of the injured peripheral nerve in vivo. However, the precise intracellular pathways involved have not been completely elucidated. Here, we show that RAGE-induced S100B secretion involves the recruitment of S100B in lipid rafts and caveolae. Moreover, we demonstrate for the first time that RAGE induces the expression of thioredoxin interacting protein (TXNIP) in SCs and the injured sciatic nerve in vivo. TXNIP is involved in the activation of p38 MAPK, CREB and NFB in SCs. TXNIP silencing partially inhibits RAGE-induced SC migration and completely abolishes RAGE-induced fibronectin and IL-1 expression. Our results support a model in which TXNIP mediates in part RAGE-induced SC migration and is required for the expression of provisional ECM and pro-inflammatory IL-1. We provide new insight on the role of the SC RAGE-TXNIP axis in the repair of injured peripheral nerves.

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“…This may also explain why stable K-CREB expression alone in TR-iBRB2 does not reduce the IGF-1-mediated fibronectin expression completely to the level of the K-CREB control cells without IGF-1 treatment ( Figure 4B). We have previously shown that CREB is also involved in ECM gene induction in renal mesangial cells by IGF-1 and under high ambient glucose condition [23,24,45] and that CREB phosphorylation is increased in diabetic renal cortex, which correlated positively with ECM gene expression in the mesangium [15,27]. In this study, we demonstrate that fibronectin and laminin γ1 expressions are increased by IGF-1 in retina endothelial cells and that the GSK-3β/CREB pathway is involved in this process ( Figure 4B and Figure S3C).…”

Section: Accepted Manuscriptmentioning

confidence: 99%

GSK-3β/CREB axis mediates IGF-1-induced ECM/adhesion molecule expression, cell cycle progression and monolayer permeability in retinal capillary endothelial cells: Implications for diabetic retinopathy

Devi

Singh²,

Hosoya³

2011

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Various growth factors and cytokines are implicated in endothelial dysfunction and blood-retinal barrier (BRB) breakdown in early diabetic retinopathy (DR). However, cellular and molecular mechanisms that may underlie the pathology of DR are not fully understood yet. We therefore examined the effect of insulin-like growth factor (IGF)-1 on ECM/adhesion molecule expression, cell cycle regulation and monolayer permeability in an endothelial cell line (TR-iBRB2). We investigate whether the action of IGF-1 (1) involves glycogen synthase kinase 3beta (GSK-3β) and cAMP responsive transcription factor (CREB) and (2) alters ECM/adhesion molecule gene expression. Treatment of TR-iBRB2 cell with IGF-1 (100ng/ml for 0-24h) increases phosphorylation of (i) Akt Thr308, and its substrates including GSK-3β at Ser9, which inactivates its kinase function, and (ii) CREB at Ser133 (activation). These phosphorylations correlate positively with enhanced expression of CREB targets such as ECM protein fibronectin and cell cycle progression factor cyclin D1. However, stable transfection of a mutant GSK3β(S9A) or a dominant negative K-CREB in TR-iBRB2 prevents IGF-1-induced fibronectin and cyclin D1 expression. Furthermore, IGF-1 reduces the level of intercellular adherence molecule VE-cadherin and increases monolayer permeability in TR-iBRB2 cells when measured by FITC-dextran leakage. The effect of IGF-1 on VE-cadherin and membrane permeability is absent in TR-iBRB2 cells expressing the GSK-3β(S9A). Similarly, K-CREB reverses IGF-1 down-regulation of VE-cadherin and up-regulation of fibronectin. These results indicate that GSK-3β/CREB axis alters ECM/adhesion molecule expression and cell cycle progression in retinal endothelial cells, and may potentially contribute to endothelial dysfunction and BRB leakage in DR.

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Overexpression of the Complementary DNA for Human Glutamine:Fructose-6-Phosphate Amidotransferase in Mesangial Cells Enhances Glucose-Induced Fibronectin Synthesis and Transcription Factor Cyclic Adenosine Monophosphate-Responsive Element Binding Phosphorylation

Cited by 3 publications

References 0 publications

Molecular mechanisms of glutamine action

Molecular mechanisms of glutamine action

RAGE–TXNIP axis is required for S100B-promoted Schwann cell migration, fibronectin expression and cytokine secretion

GSK-3β/CREB axis mediates IGF-1-induced ECM/adhesion molecule expression, cell cycle progression and monolayer permeability in retinal capillary endothelial cells: Implications for diabetic retinopathy

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