Identification of nuclear factor-κB sites in the Slc2a4 gene promoter

Furuya, Daniela Tomie; Neri, Elida Adalgisa; Poletto, Ana Claudia; Anhê, Gabriel Forato; Freitas, Helayne Soares; Campello, Raquel Saldanha; Rebouças, Nancy Amaral; Machado, Ubiratan Fabres

doi:10.1016/j.mce.2013.01.019

Cited by 41 publications

(58 citation statements)

References 19 publications

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“…Recently, NF-B was shown to act as a direct inhibitor of Slc2a4 transcription. 17 Both the p50 and p65 subunits (members of the NF-B family) can bind to sequences present in the Slc2a4 gene (−134 to −113 bp and −83 to −62 bp in the mouse gene), leading to decreased GLUT4 expression. 17 In fact, expression of this gene in the GM was decreased in the PED-o group when compared with the CN-o group (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…The NF‐κB family in mammalian cells is a homo‐ or heterodimeric complex formed by the Rel‐like domain‐containing proteins RelA (p65), RelB, NF‐κB1/p105, NF‐κB1/p50, c‐Rel, NF‐κB2/p52, and NF‐κB2/p100. The heterodimeric p50/p65 form is the most common . This transcription factor has been associated with the inhibition of Slc2a4 gene expression, which encodes the glucose transporter type 4 (GLUT4), an essential protein for glucose entry into muscle tissue cells …”

mentioning

confidence: 99%

“…The heterodimeric p50/p65 form is the most common. 17,18 This transcription factor has been associated with the inhibition of Slc2a4 gene expression, which encodes the glucose transporter type 4 (GLUT4), an essential protein for glucose entry into muscle tissue cells. 19 Epigenetic mechanisms, such as DNA methylation, can also control gene expression.…”

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confidence: 99%

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Effect of maternal periodontitis on GLUT4 and inflammatory pathway in adult offspring

Mattera

Chiba²,

Lopes

et al. 2019

Journal of Periodontology

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Background Maternal periodontal disease leads to low birth weight (LBW), insulin resistance (IR), increased TNF‐α levels, and alterations in insulin signaling in adult offspring. TNF‐α has been associated with the stimulation of IKKβ/NF‐κB, resulting in the decreased expression of GLUT4. Another mechanism that may be involved in decreasing GLUT4 expression is DNA methylation. This study aimed to evaluate in the adult offspring of rats with periodontal disease: IR, inflammatory pathways, DNA methylation, and expression of GLUT4. Methods Female Wistar rats were distributed into control and experimental periodontal disease groups. Seven days after induction of periodontal disease, both groups were mated with healthy male rats. After weaning, male offspring were distributed into control offspring (CN‐o) and periodontal disease offspring (PED‐o) groups. Body weights were measured from 0–75 days of age. At day 75, the following were measured in the offspring: IR (HOMA‐IR index); TNF‐α and NF‐κBp65 content in the gastrocnemius muscle (GM) by western blotting; IKKα/β, JNK, ERK 1/2, NF‐κBp65, and NF‐κBp50 phosphorylation status in the GM by western blotting; DNA methylation by restriction digest and real‐time PCR(qAMP); and expression of GLUT4 mRNA in the GM by real‐time PCR. Results LBW, IR, increases in TNF‐α, IKKα/β, ERK 1/2, NF‐κBp65, and NF‐κBp50 decreased expression of GLUT4 mRNA were observed in the PED‐o rats. No differences were identified in JNK phosphorylation status and DNA methylation in the evaluated regions of the GLUT4‐encoding gene Slc2a4. Conclusion Maternal periodontal disease causes LBW, IR, activation of inflammatory pathways, and decreased GLUT4 expression in the GM of adult offspring.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Effect of maternal periodontitis on GLUT4 and inflammatory pathway in adult offspring

Mattera

Chiba²,

Lopes

et al. 2019

Journal of Periodontology

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“…But, avenues to do so certainly exist. For instance, the SLC2A4 gene encoding GLUT4 is repressed by the inflammatory transcription factor NF-κB [38]. Thus, increased inflammation in CIM skeletal muscle could have let to an activation of the inflammation mediator NF-κB mediating downregulation of GLUT4.…”

Section: Discussionmentioning

confidence: 99%

Inflammation-Induced Acute Phase Response in Skeletal Muscle and Critical Illness Myopathy

et al. 2014

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ObjectivesSystemic inflammation is a major risk factor for critical-illness myopathy (CIM) but its pathogenic role in muscle is uncertain. We observed that interleukin 6 (IL-6) and serum amyloid A1 (SAA1) expression was upregulated in muscle of critically ill patients. To test the relevance of these responses we assessed inflammation and acute-phase response at early and late time points in muscle of patients at risk for CIM.DesignProspective observational clinical study and prospective animal trial.SettingTwo intensive care units (ICU) and research laboratory.Patients/Subjects33 patients with Sequential Organ Failure Assessment scores ≥8 on 3 consecutive days within 5 days in ICU were investigated. A subgroup analysis of 12 patients with, and 18 patients without CIM (non-CIM) was performed. Two consecutive biopsies from vastus lateralis were obtained at median days 5 and 15, early and late time points. Controls were 5 healthy subjects undergoing elective orthopedic surgery. A septic mouse model and cultured myoblasts were used for mechanistic analyses.Measurements and Main ResultsEarly SAA1 expression was significantly higher in skeletal muscle of CIM compared to non-CIM patients. Immunohistochemistry showed SAA1 accumulations in muscle of CIM patients at the early time point, which resolved later. SAA1 expression was induced by IL-6 and tumor necrosis factor-alpha in human and mouse myocytes in vitro. Inflammation-induced muscular SAA1 accumulation was reproduced in a sepsis mouse model.ConclusionsSkeletal muscle contributes to general inflammation and acute-phase response in CIM patients. Muscular SAA1 could be important for CIM pathogenesis.Trial RegistrationISRCTN77569430.

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“…Increased pro‐inflammatory cytokines have been related to reduced expression of the glucose transporter 4 (GLUT4) in adipose tissue and plasma . Furthermore, nuclear factor‐κB (NF‐κB), a mediator of several inflammatory effects, has been shown to repress GLUT4 protein expression, thus contributing to insulin resistance …”

Section: Introductionmentioning

confidence: 99%

Atorvastatin administered before myocardial infarction in rats improves contractility irrespective of metabolic changes

Lehnen

Tavares

et al. 2014

Clin Exp Pharmacol Physiol

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Statins have a beneficial effect after myocardial infarction, but the relationship between glucose transporters and their use before the event has not yet been studied. We assessed the effects of atorvastatin treatment pre- and post-myocardial infarction on cardiovascular function and glucose transporter 4 (GLUT4) in the heart. Wistar-Kyoto rats were treated with 20 mg/kg atorvastatin or vehicle for 14 days before coronary artery occlusion surgery (myocardial infarction) or sham surgery. Echocardiographic evaluations were carried out 48 h after myocardial infarction (protocol A) and after 7 days (protocol B), when atorvastatin was also administered. Plasma inflammatory markers and GLUT4 in the heart were also evaluated. Animals were divided into the following groups: sham-operated and vehicle (C), myocardial infarction and vehicle (I), sham-operated and atorvastatin (CAt) and myocardial infarction and atorvastatin (IAt). After 48 h, myocardial infarction induced higher left ventricular fractional shortening in IAt versus I (~ 60%, P = 0.036), and the ejection fraction was lower (protocol A ~ 37%; protocol B ~ 30%). Myocardial infarction was associated with a rise in plasma membrane GLUT4 after 48 h (~ 40%, P < 0.001), and a reduction in GLUT4 after 7 days (I 25%; IAt 49%, P < 0.001). Atorvastatin treatment for 48 h after the infarction did not change GLUT4 expression, and after 7 days it had an additional negative effect on GLUT4 content (~ 39%, P = 0.030). In conclusion, atorvastatin treatment pre- and post-myocardial infarction improved myocardial contractility after 48 h, but not after 7 days, and was not associated with an increase in GLUT4 expression.

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Identification of nuclear factor-κB sites in the Slc2a4 gene promoter

Cited by 41 publications

References 19 publications

Effect of maternal periodontitis on GLUT4 and inflammatory pathway in adult offspring

Effect of maternal periodontitis on GLUT4 and inflammatory pathway in adult offspring

Inflammation-Induced Acute Phase Response in Skeletal Muscle and Critical Illness Myopathy

Atorvastatin administered before myocardial infarction in rats improves contractility irrespective of metabolic changes

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