scholarly journals Plasma cytokine response during the postprandial period: a potential causal process in vascular disease?

2005 ◽  
Vol 93 (1) ◽  
pp. 3-9 ◽  
Author(s):  
Graham C. Burdge ◽  
Philip C. Calder
Keyword(s):  
Inflammatory Cytokines ◽  
Vascular Endothelium ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Causal Mechanism ◽  
Causal Process ◽  
Fatty Meal ◽  
Postprandial Lipaemia ◽  
Soluble Adhesion Molecules ◽  
Pro Inflammatory Cytokines

Chronic inflammation of the vascular endothelium produces endothelial dysfunction and ultimately atherogenesis. Postprandial hyperlipidaemia is an independent risk factor for cardiovascular disease. Recent studies show that the magnitude of postprandial lipaemia following a single fatty meal is negatively related to vascular function. This is associated with a transient increase in the concentrations of pro-inflammatory cytokines and soluble adhesion molecules and in pro-oxidant activity. One possible interpretation is that repeated exposure of the blood vessel wall to the activities of pro-inflammatory cytokines and pro-oxidants may damage the vascular endothelium and promote atherogenesis. Based on these results, we propose a model of a causal mechanism to explain how consumption of a fatty meal may impair vascular dysfunction.

Abstract 1123: Critical Role Of Adipose Senescence In Insulin Resistance And Vascular Dysfunction

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Masayuki Orimo ◽  
Tohru Minamino ◽  
Hideyuki Miyauchi ◽  
Kaoru Tateno ◽  
Sho Okada ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Inflammatory Cytokines ◽  
Cellular Senescence ◽  
Vascular Dysfunction ◽  
Critical Role ◽  
Serum Levels ◽  
P53 Expression ◽  
Deficient Mice ◽  
Pro Inflammatory Cytokines

Cellular senescence is originally described as the finite replicative lifespan of human somatic cells in culture. As a consequence of semi-conservative DNA replication, the extreme terminals of the chromosomes are not duplicated completely, resulting in successive shortening of telomeres with each cell division. Telomerase is a ribonucleoprotein that adds telomeres to the ends of chromosomes. Critically short telomeres are thought to trigger DNA damage response, thereby inducing cellular senescence. Accumulating evidence has suggested that senescent cells promote aging phenotypes or age-related pathologies. Here we show that adipose senescence is critically involved in the regulation of insulin resistance that underlies age-associated cardiovascular disease. The later generation of telomerase-deficient mice with short telomeres exhibited insulin resistance and vascular dysfunction when fed on a high-calorie diet. Adipose tissue of these mice revealed senescence-like phenotypes such as an increase in neutral β galactosidase activity and upregulation of p53 and pro-inflammatory cytokines. Serum levels of pro-inflammatory cytokines were markedly elevated in telomerase-deficient mice and treatment of these mice with a neutralizing antibody against TNF-α significantly improved insulin and glucose intolerance. Removal of senescent adipose tissue reduced serum levels of pro-inflammatory cytokines and thereby improved insulin resistance in telomerase-deficient mice. Conversely, implantation of senescent adipose tissue to wild-type mice impaired insulin sensitivity and glucose tolerance in recipients. Introduction of telomere dysfunction to young adipose tissue markedly upregulated p53 expression and increased the production of pro-inflammatory cytokines. Inhibition of p53 activity significantly improved senescence-like phenotypes of adipose tissue, insulin resistance, and vascular dysfunction in telomerase-deficient mice. These results disclose a novel mechanism of insulin resistance and suggest that adipose senescence is a potential therapeutic target for the treatment of diabetes and diabetic vasculopathy.

scholarly journals Diabetes and the maternal resistance vasculature

2001 ◽  
Vol 101 (6) ◽  
pp. 719-729 ◽  
Author(s):  
Christine ANG ◽  
Mary Ann LUMSDEN
Keyword(s):  
Blood Flow ◽  
Vascular Endothelium ◽  
Pregnancy Outcomes ◽  
Vascular Function ◽  
Vascular Reactivity ◽  
Vascular Dysfunction ◽  
Tissue Perfusion ◽  
Endocrine Disorder ◽  
Patient Morbidity ◽  
Adverse Pregnancy

Diabetes is the most common endocrine disorder worldwide, with complications that include the development of both macro- and micro-vascular disease that contribute significantly to patient morbidity and mortality. The severity of diabetic complications is amplified during pregnancy, resulting in a higher incidence of adverse pregnancy outcomes such as pre-eclampsia, placental insufficiency and stillbirth than in non-diabetics. Vascular dysfunction is thought to underlie many of these complications, with the greatest impact occurring at the level of the resistance vasculature, where alterations in vascular reactivity can significantly affect blood flow and tissue perfusion. It is likely that problems associated with diabetic pregnancies are related, in part, to abnormal vascular function, particularly dysfunction of the vascular endothelium.

scholarly journals Baroreceptor denervation reduces inflammatory status and worsens cardiovascular collapse during systemic inflammation

2019 ◽  
Author(s):  
Mateus R. Amorim ◽  
Júnia L. de Deus ◽  
Camila A. Pereira ◽  
Luiz E. V. da Silva ◽  
Gabriela S. Borges ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Vessels ◽  
Inflammatory Cytokines ◽  
Systemic Inflammation ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Cardiovascular Collapse ◽  
Inflammatory Status ◽  
Resistance Vessels ◽  
Autonomic Cardiovascular Control

ABSTRACTBeyond the regulation of cardiovascular function, baroreceptor afferents play polymodal roles. We hypothesized that baroreceptor denervation affects lipopolysaccharide (LPS)-induced systemic inflammation (SI) and hemodynamic collapse in conscious rats, and that these parameters are interconnected. We combine: a) hemodynamic and thermoregulatory recordings after LPS administration at a septic-like dose b) analysis of the cardiovascular complexity, c) evaluation of vascular function in mesenteric resistance vessels, and d) measurements of inflammatory cytokines (plasma and spleen). LPS-induced drop in blood pressure was higher in sino-aortic denervated (SAD) rats. LPS-induced hemodynamic collapse was associated with SAD-dependent autonomic disbalance. LPS-induced vascular dysfunction was not affected by SAD. Surprisingly, SAD blunted LPS-induced surges of plasma and spleen cytokines. These data indicate that sino-aortic afferents are key to alleviate LPS-induced cardiovascular collapse, affecting the autonomic cardiovascular control, without affecting resistance blood vessels. Moreover, baroreflex modulation of the LPS-induced SI and hemodynamic collapse seem not to be interconnected.

Abstract 61: Adipose Tissue Specific HO-1 Induction Regulates the Crosstalk between Wnt and β-catenin Pathways and Leads to Restoration of Vascular Endothelial Function in Mice Fed a High Fat Diet

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Jian Cao ◽  
Stephen J Peterson ◽  
Michal L Schwartzman ◽  
Komal Sodhi ◽  
Rita Rezzani ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Inflammatory Cytokines ◽  
High Fat Diet ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Subcutaneous Fat ◽  
Heme Oxygenase 1 ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Intracardiac Injection

The principal goal of the present study is to examine the contributions of adipocyte specific over expression of the cytoprotective gene heme oxygenase-1 (HO-1) in modulating vascular function in an animal model of diet induced obesity. A lentiviral construct of the human HO-1 was synthesized under the control of an aP2-activated promoter so as to ensure HO-1 targeting to murine adipocytes. Lentiviruses (50 μl, 2x109 TU/ml in saline) were injected into the C57BL/6 mice by a single intracardiac injection. Mice (6-7 wks old) were divided into 4 groups: Control, high fat diet (HF) mice receiving the control Lenti-aP2-GFP (HF-GFP) and high fat diet mice receiving the lenti-aP2-HO-1 (HF-HO-1) with and without treatment with SnMP. Transduction of lenti-aP2-HO-1 increased human HO-1 expression in adipose tissues without affecting endogenous mice HO-1 (p<0.01). In mice fed a HF diet, lenti-aP2-HO-1 transduction attenuated the increases in body weight (from 52.0±1.0 g to 35.6±2.1g; p<0.01), blood glucose (from 255±3.5 g to 140±2.9mg/dl), blood pressure (from 135±2.8mmHg to 101±2.2mmHg; p<0.01) and inflammatory cytokines as well as the content of both visceral (from 5.5±0.15g to 2.9±0.22g; p<0.05) and subcutaneous fat (p<0.05). Transduction of lenti-aP2-HO-1 increased the numbers of adipocytes of small cell size (p<0.05), insulin sensitivity (p<0.05), adiponectin levels (from 32.4±1.9μg/ml to 19.9±2.1μg/ml; p<0.05) as well as vascular relaxation to acetylcholine ( p<0.05) compared to HF mice administered the lenti-aP2- GFP. Adipocytes of mice fed a HF diet expressed high levels of PPARγ, aP2, C/EBP and Wnt5b proteins and displayed marked increases in Peg1/Mest (p<0.03). Lenti-aP2-HO-1 transduction lowered the elevated levels of these proteins and increased Shh, Wnt10b and β-catenin (p<0.05). Inhibition of HO activity by administration of tin mesoporphyrin (SnMP) to HF-fed mice transduced with the lenti-aP2-HO-1 reversed the decrease in Peg 1/Mest, TNFα and MCP-1 levels. This novel study demonstrate that adipocyte-specific overexpression of HO-1 attenuates HF-mediated adiposity and vascular dysfunction, increases insulin sensitivity and improves adipocyte function by increasing adiponectin, Shh and WNT10b and decreasing inflammatory cytokines.

Cytokine synergy, collagenases and cartilage collagen breakdown

2003 ◽  
Vol 70 ◽  
pp. 125-133 ◽  
Author(s):  
Tim E. Cawston ◽  
Jenny M. Milner ◽  
Jon B. Catterall ◽  
Andrew D. Rowan
Keyword(s):  
Matrix Metalloproteinases ◽  
Inflammatory Cytokines ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
And Cartilage ◽  
Pro Inflammatory Cytokines

We have investigated proteinases that degrade cartilage collagen. We show that pro-inflammatory cytokines act synergistically with oncastatin M to promote cartilage collagen resorption by the up-regulation and activation of matrix metalloproteinases (MMPs). The precise mechanisms are not known, but involve the up-regulation of c-fos, which binds to MMP promoters at a proximal activator protein-1 (AP-1) site. This markedly up-regulates transcription and leads to higher levels of active MMP proteins.

Inhibition of Pro-Inflammatory Cytokine Secretion by Select Antioxidants in Human Coronary Artery Endothelial Cells

2020 ◽  
Vol 90 (1-2) ◽  
pp. 103-112 ◽  
Author(s):  
Michael J. Haas ◽  
Marilu Jurado-Flores ◽  
Ramadan Hammoud ◽  
Victoria Feng ◽  
Krista Gonzales ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ascorbic Acid ◽  
Coronary Artery ◽  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Culture Media ◽  
Cytokine Secretion ◽  
Human Coronary Artery ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

Abstract. Inflammatory and oxidative stress in endothelial cells are implicated in the pathogenesis of premature atherosclerosis in diabetes. To determine whether high-dextrose concentrations induce the expression of pro-inflammatory cytokines, human coronary artery endothelial cells (HCAEC) were exposed to either 5.5 or 27.5 mM dextrose for 24-hours and interleukin-1β (IL-1β), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor α (TNF α) levels were measured by enzyme immunoassays. To determine the effect of antioxidants on inflammatory cytokine secretion, cells were also treated with α-tocopherol, ascorbic acid, and the glutathione peroxidase mimetic ebselen. Only the concentration of IL-1β in culture media from cells exposed to 27.5 mM dextrose increased relative to cells maintained in 5.5 mM dextrose. Treatment with α-tocopherol (10, 100, and 1,000 μM) and ascorbic acid (15, 150, and 1,500 μM) at the same time that the dextrose was added reduced IL-1β, IL-6, and IL-8 levels in culture media from cells maintained at 5.5 mM dextrose but had no effect on IL-1β, IL-6, and IL-8 levels in cells exposed to 27.5 mM dextrose. However, ebselen treatment reduced IL-1β, IL-6, and IL-8 levels in cells maintained in either 5.5 or 27.5 mM dextrose. IL-2 and TNF α concentrations in culture media were below the limit of detection under all experimental conditions studied suggesting that these cells may not synthesize detectable quantities of these cytokines. These results suggest that dextrose at certain concentrations may increase IL-1β levels and that antioxidants have differential effects on suppressing the secretion of pro-inflammatory cytokines in HCAEC.

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