Fabp4 contributes toward regulating inflammatory gene expression and oxidative stress in Ctenopharyngodon idella

2022 ◽  
pp. 110715
Author(s):  
Cai-xia Lei ◽  
Yu-jing Xie ◽  
Sheng-jie Li ◽  
Peng-Jiang ◽  
Jin-xing Du
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Ctenopharyngodon Idella ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
And Oxidative Stress

scholarly journals Enhanced vulnerability to oxidative stress and induction of inflammatory gene expression in 3‐phosphoglycerate dehydrogenase‐deficient fibroblasts

FEBS Open Bio ◽  
2018 ◽  
Vol 8 (6) ◽  
pp. 914-922 ◽  
Author(s):  
Momoko Hamano ◽  
Yurina Haraguchi ◽  
Tomoko Sayano ◽  
Chong Zyao ◽  
Yashiho Arimoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Phosphoglycerate Dehydrogenase

Oxidative stress and macrophage function: a failure to resolve the inflammatory response

2007 ◽  
Vol 35 (2) ◽  
pp. 284-287 ◽  
Author(s):  
P. Kirkham
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Inflammatory Response ◽  
Carbonyl Stress ◽  
Apoptotic Cells ◽  
Inflammatory Gene Expression ◽  
Macrophage Function ◽  
Inflammatory Gene ◽  
Ecm Proteins ◽  
Inflammatory State

The suppression of pro-inflammatory gene expression along with the clearance of apoptotic cells by phagocytosis can play an important role in resolving the inflammatory response. Any impairment of these processes can therefore lead to a chronic inflammatory state. Oxidative stress can have both direct and indirect effects on macrophage function. This mini-review highlights a mechanism through which oxidative stress via the production of reactive carbonyls alters the ECM (extracellular matrix) environment of macrophages, thereby altering their behaviour. Carbonyl modification of ECM proteins causes increased macrophage adhesion and activation through receptors that are also involved in phagocytosis. Moreover, interaction of macrophages with these carbonyl-modified ECM proteins leads to decreased phagocytic activity towards apoptotic cells. At a more direct level, both oxidative and carbonyl stress inhibits activity of the transcriptional co-repressor HDAC-2 (histone deacetylase 2), which under normoxic conditions helps to suppress pro-inflammatory gene expression. Consequently, macrophages activated under conditions of oxidative or carbonyl stress can lead to a more enhanced inflammatory response. Coupled with an impairment of the phagocytic response, this can lead to ineffective clearance of apoptotic cells and secondary necrosis, with the result being failure to resolve the inflammatory response and the establishment of a chronic inflammatory state.

scholarly journals Gene Expression Profiling and Functional Characterization of Macrophages in Response to Circulatory Microparticles Produced during Trypanosoma cruzi Infection and Chagas Disease

2016 ◽  
Vol 9 (2) ◽  
pp. 203-216 ◽  
Author(s):  
Imran H. Chowdhury ◽  
Sue-jie Koo ◽  
Shivali Gupta ◽  
Lisa Yi Liang ◽  
Bojlul Bahar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Trypanosoma Cruzi ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Nitrosative Stress ◽  
Disease State ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Ifn Γ

Background: Chronic inflammation and oxidative stress are hallmarks of chagasic cardiomyopathy (CCM). In this study, we determined if microparticles (MPs) generated during Trypanosoma cruzi (Tc) infection carry the host's signature of the inflammatory/oxidative state and provide information regarding the progression of clinical disease. Methods: MPs were harvested from supernatants of human peripheral blood mononuclear cells in vitro incubated with Tc (control: LPS treated), plasma of seropositive humans with a clinically asymptomatic (CA) or symptomatic (CS) disease state (vs. normal/healthy [NH] controls), and plasma of mice immunized with a protective vaccine before challenge infection (control: unvaccinated/infected). Macrophages (mφs) were incubated with MPs, and we probed the gene expression profile using the inflammatory signaling cascade and cytokine/chemokine arrays, phenotypic markers of mφ activation by flow cytometry, cytokine profile by means of an ELISA and Bioplex assay, and oxidative/nitrosative stress and mitotoxicity by means of colorimetric and fluorometric assays. Results:Tc- and LPS-induced MPs stimulated proliferation, inflammatory gene expression profile, and nitric oxide (∙NO) release in human THP-1 mφs. LPS-MPs were more immunostimulatory than Tc-MPs. Endothelial cells, T lymphocytes, and mφs were the major source of MPs shed in the plasma of chagasic humans and experimentally infected mice. The CS and CA (vs. NH) MPs elicited >2-fold increase in NO and mitochondrial oxidative stress in THP-1 mφs; however, CS (vs. CA) MPs elicited a more pronounced and disease-state-specific inflammatory gene expression profile (IKBKB, NR3C1, and TIRAP vs. CCR4, EGR2, and CCL3), cytokine release (IL-2 + IFN-γ > GCSF), and surface markers of mφ activation (CD14 and CD16). The circulatory MPs of nonvaccinated/infected mice induced 7.5-fold and 40% increases in ∙NO and IFN-γ production, respectively, while these responses were abolished when RAW264.7 mφs were incubated with circulatory MPs of vaccinated/infected mice. Conclusion: Circulating MPs reflect in vivo levels of an oxidative, nitrosative, and inflammatory state, and have potential utility in evaluating disease severity and the efficacy of vaccines and drug therapies against CCM.

scholarly journals Longevity is associated with increased vascular resistance to high glucose-induced oxidative stress and inflammatory gene expression in Peromyscus leucopus

2009 ◽  
Vol 296 (4) ◽  
pp. H946-H956 ◽  
Author(s):  
Nazar Labinskyy ◽  
Partha Mukhopadhyay ◽  
Janos Toth ◽  
Gabor Szalai ◽  
Monika Veres ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Steady State ◽  
High Glucose ◽  
Peromyscus Leucopus ◽  
Metabolic Stress ◽  
Ros Generation ◽  
Vascular Aging ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

Vascular aging is characterized by increased oxidative stress and proinflammatory phenotypic alterations. Metabolic stress, such as hyperglycemia in diabetes, is known to increase the production of ROS and promote inflammatory gene expression, accelerating vascular aging. The oxidative stress hypothesis of aging predicts that vascular cells of long-lived species exhibit lower steady-state production of ROS and/or superior resistance to the prooxidant effects of metabolic stress. We tested this hypothesis using two taxonomically related rodents, the white-footed mouse ( Peromyscus leucopus) and the house mouse ( Mus musculus), which show a more than twofold difference in maximum lifespan potential (8.2 and 3.5 yr, respectively). We compared interspecies differences in steady-state and high glucose (HG; 30 mmol/l)-induced production of O2•− and H2O2, endothelial function, mitochondrial ROS generation, and inflammatory gene expression in cultured aortic segments. In P. leucopus aortas, steady-state endothelial O2•− and H2O2 production and ROS generation by mitochondria were less than in M. musculus vessels. Furthermore, vessels of P. leucopus were more resistant to the prooxidant effects of HG. Primary fibroblasts from P. leucopus also exhibited less steady-state and HG-induced ROS production than M. musculus cells. In M. musculus arteries, HG elicited significant upregulation of inflammatory markers (TNF-α, IL-6, ICAM-1, VCAM, and monocyte chemoattractant protein-1). In contrast, the proinflammatory effects of HG were blunted in P. leucopus vessels. Thus, increased life span potential in P. leucopus is associated with decreased cellular ROS generation and increased resistance to prooxidant and proinflammatory effects of metabolic stress, which accord with predictions of the oxidative stress hypothesis of aging.

scholarly journals Bisphenol-A induced oxidative stress, inflammatory gene expression, and metabolic and histopathological changes in male Wistar albino rats: protective role of boron

2019 ◽  
Vol 8 (2) ◽  
pp. 262-269 ◽  
Author(s):  
Ulas Acaroz ◽  
Sinan Ince ◽  
Damla Arslan-Acaroz ◽  
Zeki Gurler ◽  
Hasan Huseyin Demirel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Bisphenol A ◽  
Protective Role ◽  
Albino Rats ◽  
Histopathological Changes ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Wistar Albino Rats

Boron reversed Bisphenol-A induced alterations.

scholarly journals Changes in LDL Oxidative Status and Oxidative and Inflammatory Gene Expression after Red Wine Intake in Healthy People: A Randomized Trial

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Laura Di Renzo ◽  
Luigi Tonino Marsella ◽  
Alberto Carraro ◽  
Roberto Valente ◽  
Paola Gualtieri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Red Wine ◽  
Protective Action ◽  
Nutritional Intervention ◽  
Ldl Oxidation ◽  
Inflammatory Gene Expression ◽  
Stress Related Genes ◽  
And Oxidative Stress ◽  
Increased Susceptibility

Postprandial oxidative stress is characterized by an increased susceptibility of the organism towards oxidative damage after consumption of a meal rich in lipids and/or carbohydrates. Micronutrients modulate immune system and exert a protective action by reducing low density lipoproteins (LDL) oxidation via induction of antioxidant enzymes. We evaluated the gene expression of oxidative stress (HOSp), inflammasome (HIp), and human drug metabolism pathways (HDM) and ox-LDL level at baseline and after the intake of red wine naturally enriched with resveratrol (NPVRW), in association with or without a McDonald’s meal (McDM). The ox-LDL levels significantly increase comparing baseline (B)versusMcDM and decreased comparing McDMversusMcDM + NPVRW (P≤0.05). Percentages of significant genes expressed after each nutritional intervention were the following: (1) BversusMcDM, 2.88% HOSp, 2.40% of HIp, and 3.37% of HDMp; (2) BversusMcDM + NPVRW, 1.44% of HOSp, 4.81% of HIp, and 0.96% of HDMp; (3) McDMversusMcDM + NPVRW, 2.40% of HOSp, 2.40% of HIp, and 5.77% of HDMp; (4) BversusNPVRW, 4.80% HOSp, 3.85% HIp, and 3.85% HDMp. NPVRW intake reduced postprandial ox-LDL and the expression of inflammation and oxidative stress related genes. Chronic studies on larger population are necessary before definitive conclusions.

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