Low expression of the GILZ may contribute to adipose inflammation and altered adipokine production in human obesity

Lee, Mi‐Jeong; Yang, Rongze; Karastergiou, Kalypso; Smith, Steven R.; Chang, Jeffery R.; Gong, Da-Wei; Fried, Susan K.

doi:10.1194/jlr.m067728

Cited by 15 publications

(7 citation statements)

References 41 publications

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“…Патогенетическая роль гиперлептинемии реализуется через влияние на гемодинамику, функцию эндотелия, углеводный обмен, окислительную модификацию липопротеинов плазмы крови. Лептин оказывает и другие проатерогенные эффекты, участвуя в процессах гемостаза, активации тромбоцитов, воспалении, гипертрофии гладкомышечных клеток, что, в свою очередь, способствует ремоделированию сердца и сосудов, значительно повышая риск ИБС и многососудистого поражения коронарных артерий [38,39,40].…”

Section: Discussionunclassified

Subcutaneous and Epicardial Adipose Tissue Leptin Gene Expression in Coronary Artery Disease Patient

Полякова

Колодина

Miroshnikova

et al. 2019

Transl. med. (Print)

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Objective. To assess the expression of the leptin gene (LEP) in the epicardial (EAT) and subcutaneous (SAT) adipose tissue in coronary artery disease (CAD) patients.Methods. 107 people were examined: 87 with CAD (57 men, 30 women), 20 without CAD (10 men, 10 women). Biopsy of EAT, SAT, coronary angiography, heart computed tomography, blood leptin levels were estimate, mRNA expression of the LEP gene evaluated by PCR.Results. In CAD patients with multivessel coronary artery lesion, the level of blood leptin is the highest. The expression of the LEP gene in EAT is higher in men than in women, in men with CAD higher than in non-coronary artery disease patients, and with a multivascular coronary lesion higher than in a 1–2 vascular lesion. Expression of the LEP gene in EAT in women with CAD is higher than with no CAD, and does not depend on the severity of coronary atherosclerosis. In SAT, LEP gene expression in men with CAD is higher than without CAD; women with CAD are lower than without CAD. Expression of the LEP gene in SAT is higher in men with a multivascular lesion than in 1–2 vascular lesion, and lower in women with a multivascular damage.Conclusions. The expression of the leptin gene in women is higher in SAT, and in men in EAT. Expression of the leptin gene in EAT with CAD is higher than without CAD. The expression of the leptin gene in SAT in men with CAD, especially with multivessel lesions, is higher than without coronary artery disease.

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Section: Discussionunclassified

Subcutaneous and Epicardial Adipose Tissue Leptin Gene Expression in Coronary Artery Disease Patient

Полякова

Колодина

Miroshnikova

et al. 2019

Transl. med. (Print)

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“…It has also been shown that GILZ dampens the pro-inflammatory effects of TNFα in human adipocytes by inhibiting p65/NF-κB nuclear translocation (Lee et al, 2016).…”

Section: Gilz Interaction With Nf-κb and Mapk/erk Pathways In Inflammmentioning

confidence: 99%

Glucocorticoid-Induced Leucine Zipper: A Novel Anti-inflammatory Molecule

et al. 2019

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Glucocorticoids (GCs) are the most commonly used drugs for treatment of autoimmune and inflammatory diseases. Their efficacy is due to their ability to bind cytoplasmic receptors (glucocorticoid receptors, GR) and other cytoplasmic proteins, thus regulating gene expression. Although GCs are potent life-saving drugs, their therapeutic effects are transitory and chronic use of GCs is accompanied by serious side effects. Therefore, new drugs are needed to replace GCs. We have identified a gene, glucocorticoid-induced leucine zipper (GILZ or tsc22d3), that is rapidly and invariably induced by GCs. Human GILZ is a 135-amino acid protein that mediates many GC effects, including inhibition of the NF-κB and MAPK pathways. Similar to GCs, GILZ exerts anti-inflammatory activity in experimental disease models, including inflammatory bowel diseases and arthritis. While transgenic mice that overexpress GILZ are more resistant, GILZ knockout mice develop worse inflammatory diseases. Moreover, the anti-inflammatory effect of GCs is attenuated in GILZ-deficient mice. Importantly, in vivo delivery of recombinant GILZ protein cured colitis and facilitated resolution of lipopolysaccharide-induced inflammation without apparent toxic effects. A synthetic GILZ-derived peptide, corresponding to the GILZ region that interacts with NF-κB, was able to suppress experimental autoimmune encephalomyelitis. Collectively, these findings indicate that GILZ is an anti-inflammatory molecule that may serve as the basis for designing new therapeutic approaches to inflammatory diseases.

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“…GILZ indicates the activation of downstream GR signaling pathways, 61 whereby GILZ mRNA and protein levels are correlated in various tissues and have thus been used interchangeably. [102][103][104] We have here identified that Gilz was exclusively downregulated by stress challenge in female lungs, indicating a lower response to glucocorticoids in female fetal lungs. This may account for the altered lung development that we also described, because glucocorticoids are pivotal to fetal lung maturation.…”

Section: Discussionmentioning

confidence: 66%

A prenatally disrupted airway epithelium orchestrates the fetal origin of asthma in mice

Zazara

Wegmann

Giannou

et al. 2020

Journal of Allergy and Clinical Immunology

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Low expression of the GILZ may contribute to adipose inflammation and altered adipokine production in human obesity

Cited by 15 publications

References 41 publications

Subcutaneous and Epicardial Adipose Tissue Leptin Gene Expression in Coronary Artery Disease Patient

Subcutaneous and Epicardial Adipose Tissue Leptin Gene Expression in Coronary Artery Disease Patient

Glucocorticoid-Induced Leucine Zipper: A Novel Anti-inflammatory Molecule

A prenatally disrupted airway epithelium orchestrates the fetal origin of asthma in mice

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