scholarly journals In response to oxidative stress, the expression of inflammatory cytokines and antioxidant enzymes are impaired in placenta, but not adipose tissue, of women with gestational diabetes

2009 ◽  
Vol 204 (1) ◽  
pp. 75-84 ◽  
Author(s):  
Martha Lappas ◽  
Amberlee Mittion ◽  
Michael Permezel
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Pregnant Women ◽  
Mrna Expression ◽  
Human Placenta ◽  
Cytokine Release ◽  
Antioxidant Gene ◽  
Antioxidant Gene Expression

In response to oxidative stress, gestational diabetes mellitus (GDM) placenta releases less 8-isoprostane and tumour necrosis factor (TNF) α. The effect of oxidative stress on other cytokines and antioxidant gene expressions are unknown. The aim of this study is to further explore the antioxidant status and effect of oxidative stress in GDM tissue. Human placenta, omental and subcutaneous adipose tissue from women with and without GDM were exposed to hypoxanthine (HX)/xanthine oxidase (XO). Cytokine release was analysed by ELISA and cytokine and antioxidant gene expression by RT-PCR. Catalase (CAT) and glutathione reductase (GSR) mRNA expression was higher in GDM (n=18) compared with normal (n=23) placenta. There was no difference in glutathione peroxidase and superoxide dismutase mRNA expression. Antioxidant gene expression was unaltered between normal (n=18) and GDM (n=10) adipose tissue. HX/XO treatment significantly stimulated cytokine release (13/16 cytokines) and cytokine mRNA expression, and decreased antioxidant gene expression (CAT and GSR) in human placenta from normal pregnant women. In GDM placenta, HX/XO only significantly increased the release of 3/16 cytokines, while there was no effect on antioxidant gene expression. In normal and GDM adipose tissues, HX/XO increased proinflammatory cytokine and 8-isoprostane release, while there was no change in antioxidant gene expression. GDM placenta is characterised by increased antioxidant gene expression, and is less responsive to exogenous oxidative stress than tissues obtained from normal pregnant women. This may represent a protective or adaptive mechanism to prevent damage from further oxidative insult in utero as indicated by increased tissue antioxidant expression.

scholarly journals Release and regulation of leptin, resistin and adiponectin from human placenta, fetal membranes, and maternal adipose tissue and skeletal muscle from normal and gestational diabetes mellitus-complicated pregnancies

2005 ◽  
Vol 186 (3) ◽  
pp. 457-465 ◽  
Author(s):  
Martha Lappas ◽  
Kirin Yee ◽  
Michael Permezel ◽  
Gregory E Rice
Keyword(s):  
Diabetes Mellitus ◽  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Pregnant Women ◽  
Human Placenta ◽  
Fetal Membranes ◽  
Maternal Body Mass Index ◽  
Tnf Α

The aim of this study was to determine the release and regulation of leptin, resistin and adiponectin from human placenta and fetal membranes, and maternal subcutaneous adipose tissue and skeletal muscle obtained from normal and gestational diabetes mellitus (GDM)-complicated pregnancies at the time of Cesarean section. Tissue explants were incubated in the absence (basal control) or presence of 10 μg/ml lipopolysaccharide (LPS), 10, 20 or 40 ng/ml tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-8, 1 μM phorbol myristate acetate, 10, 20 and 40 mM glucose, 0.1, 1 and 10 μM insulin and 0.1 1 and 10 μM dexamethasone, progesterone and estrogen. After an 18-h incubation, the medium was collected and the release of leptin, resistin and adiponectin was quantified by ELISA. Human gestational tissues and maternal tissues released immunoreactive leptin, resistin and adiponectin; however, there was no difference in the release of either resistin or adiponectin between normal pregnant women and women with gestational diabetes. The release of leptin was significantly higher in placenta, amnion and choriodecidua obtained from normal pregnant women compared with women with GDM. However, in maternal tissues, the situation was reversed, with adipose tissue and skeletal muscle obtained from women with GDM releasing significantly greater amounts of leptin. In adipose tissue and skeletal muscle the release of leptin was significantly greater in insulin-controlled GDM compared with diet-controlled GDM, and leptin release from adipose tissue was significantly correlated with maternal body mass index. In all tissues tested, there was no effect of incubation with LPS, IL-6, IL-8 or TNF-α on leptin, resistin or adiponectin release. PMA significantly increased the release of resistin from placenta and adipose tissue. Insulin increased placental resistin release, whereas the hormones dexamethasone, progesterone and estrogen significantly decreased placental resistin release. The data presented in this study demonstrate that dysregulation of leptin metabolism and/or function in the placenta may be implicated in the pathogenesis of GDM. Furthermore, resistin release is greatly affected by a variety of inflammatory mediators and hormones.

scholarly journals The Antitumor Agent Imexon Activates Antioxidant Gene Expression: Evidence for an Oxidative Stress Response

2007 ◽  
Vol 13 (11) ◽  
pp. 3388-3394 ◽  
Author(s):  
Amanda F. Baker ◽  
Terry Landowski ◽  
Robert Dorr ◽  
Wendy R. Tate ◽  
Jaime M.C. Gard ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Stress Response ◽  
Antitumor Agent ◽  
Oxidative Stress Response ◽  
Antioxidant Gene ◽  
Antioxidant Gene Expression ◽  
Expression Evidence

scholarly journals Changes in Plasma Concentrations and mRNA Expression of Hepatokines Fetuin A, Fetuin B and FGF21 in Physiological Pregnancy and Gestational Diabetes Mellitus

2018 ◽  
pp. S531-S542 ◽  
Author(s):  
P. ŠIMJÁK ◽  
A. CINKAJZLOVÁ ◽  
K. ANDERLOVÁ ◽  
J. KLOUČKOVÁ ◽  
H. KRATOCHVÍLOVÁ ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Pregnant Women ◽  
Mrna Expression ◽  
Plasma Concentrations ◽  
Fibroblast Growth Factor 21 ◽  
Fetuin A ◽  
Reactive Protein ◽  
Group 12 ◽  
Tnf Α

We measured plasma concentrations, adipose tissue and placental mRNA expression of hepatokines fetuin A, fetuin B and fibroblast growth factor 21 (FGF21) in 12 healthy pregnant women (P group), 12 pregnant women with gestational diabetes (GDM) and 10 healthy non-pregnant women (N group) to explore their potential role in the etiopathogenesis of GDM. GDM and P group had comparable BMI, C-reactive protein (CRP) and glycated hemoglobin levels while IL-10 and TNF-α levels were higher in GDM group. Fetuin A and fetuin B levels were higher in pregnancy as compared to N group and decreased after delivery with no apparent influence of GDM. In contrast, the pattern of changes of circulating FGF21 levels differed between GDM and P group. Fetuin A concentrations positively correlated with CRP, TNF-α mRNA expression in adipose tissue and IL-6 mRNA expression in placenta. Fetuin B positively correlated with CRP. FGF21 levels correlated positively with IFN-γ mRNA in adipose tissue and inversely with IL-8 mRNA in the placenta. Taken together, fetuin A and fetuin B levels were increased during pregnancy regardless of the presence of GDM. In contrast, FGF21 patterns differed between healthy pregnant women and GDM patients suggesting a possible role of this hepatokine in the etiopathogenesis of GDM.

scholarly journals BRCA1 Induces Antioxidant Gene Expression and Resistance to Oxidative Stress

2004 ◽  
Vol 64 (21) ◽  
pp. 7893-7909 ◽  
Author(s):  
Insoo Bae ◽  
Saijun Fan ◽  
Qinghui Meng ◽  
Jeong Keun Rih ◽  
Hee Jong Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Antioxidant Gene ◽  
Antioxidant Gene Expression

scholarly journals AGE-Rich Bread Crust Extract Boosts Oxidative Stress Interception via Stimulation of the NRF2 Pathway

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 3874
Author(s):  
Kristin Wächter ◽  
Alexander Navarrete Santos ◽  
Anne Großkopf ◽  
Tim Baldensperger ◽  
Marcus A. Glomb ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Antioxidant Gene ◽  
Nrf2 Pathway ◽  
Cellular Models ◽  
Nrf2 Signaling Pathway ◽  
Bread Crust ◽  
Antioxidant Gene Expression

Advanced glycation end products (AGEs) result from a non-enzymatic reaction of proteins with reactive carbohydrates. Heat-processed food, such as bread, contains high amounts of AGEs. The activation of the NF-κB signaling pathway by bread crust extract (BCE) is well understood. However, it is largely unknown whether NRF2, the master regulator of oxidative stress resistance in mammalian cells, is affected by BCE. We have investigated the molecular mechanisms by which BCE induces antioxidant gene expression in cellular models. Our data showed that soluble extracts from bread crust are capable of stimulating the NRF2 signaling pathway. Furthermore, NRF2 pathway activation was confirmed by microarray and reporter-cell analyses. QRT-PCR measurements and Western blot analyses indicated an induction of antioxidative genes such as HMOX1, GCLM and NQO1 upon BCE treatment. Moreover, BCE pretreated cells had a survival advantage compared to control cells when exposed to oxidative stress. BCE induces phosphorylation of AKT and ERK kinase in EA.hy926 cells. By mass spectrometry, several new, potentially active modifications in BCE were identified. Our findings indicate that BCE activates NRF2-dependent antioxidant gene expression, thus provoking a protection mechanism against oxidative stress-mediated tissue injury. Hence, BCE can be considered as functional food with antioxidative and cardioprotective potential.

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