A Systems Toxicology Approach to Investigating the Cardiovascular Effects of Cigarette Smoke and Environmental Pollutants in ApoE-Deficient Mice

2015 ◽  
pp. 345-370
Author(s):  
Héctor De León ◽  
Stephanie Boue ◽  
Manuel C. Peitsch ◽  
Julia Hoeng
Keyword(s):  
Cigarette Smoke ◽  
Environmental Pollutants ◽  
Cardiovascular Effects ◽  
Systems Toxicology ◽  
Deficient Mice

Computers and Iatrocomplexities

1966 ◽  
Vol 05 (04) ◽  
pp. 167-171 ◽  
Author(s):  
L. E. Faer
Keyword(s):  
Twentieth Century ◽  
Cigarette Smoke ◽  
Environmental Pollutants ◽  
Genetic Composition ◽  
Koch’S Postulates ◽  
Lung Malignancies ◽  
Causative Agents ◽  
Disease Study ◽  
Multiple Etiology ◽  
Great Advance

Developments of disease hypotheses and conceptions of disease as philosophic entities have shown bursts of great advance. One just concluded includes emergence of bacteriology and virology culminating in Koch’s Postulates, which in the twentieth century were primary bases for disease study and colored all approaches to medicine.With recent extraordinary advances in technology, medicine faces great new obligations demanding fresh approaches and untrammeled thinking for solution of problems posed. It is clear that any approach to diseases and disabilities induced by exposures to environmental pollutants must take multiple etiology into account. For example, contributing to causation of lung malignancies one must list usual dusts, radioactivity, smog, auto exhausts, cigarette smoke and genetic composition. Consideration of plural factors in genesis of environmentally associated disease leads to the hypothesis of the incremental insult, a complex and difficult conception in which must be included provision for multiple causative agents, each contributing but a fraction toward total etiology^ Computers developed to their present refinement provide necessary tools for whatever complexity required to spawn and fructify hypotheses of inter-relating associations of incremental insults leading to pathology.

Atherogenic and pulmonary responses of ApoE- and LDL receptor-deficient mice to sidestream cigarette smoke

Toxicology ◽  
2012 ◽  
Vol 299 (2-3) ◽  
pp. 133-138 ◽  
Author(s):  
Sung Gu Han ◽  
Deborah A. Howatt ◽  
Alan Daugherty ◽  
C. Gary Gairola
Keyword(s):  
Cigarette Smoke ◽  
Ldl Receptor ◽  
Deficient Mice

The effects of fish oil consumption on cardiovascular remodeling in ApoE deficient mice

2013 ◽  
Vol 91 (11) ◽  
pp. 960-965 ◽  
Author(s):  
Kelby Cleverley ◽  
Xiaozhou Du ◽  
Sheena Premecz ◽  
Khuong Le ◽  
Matthew Zeglinski ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Fatty Acid ◽  
Fish Oil ◽  
High Fat Diet ◽  
Cardiovascular Effects ◽  
Left Ventricular ◽  
Omega 3 ◽  
High Fat ◽  
Omega 3 Fatty Acid ◽  
Deficient Mice

Owing to their spontaneous development of atherosclerosis, apolipoprotein E knockout mice (ApoEKO) are one of the best studied animal models for this disease. Little is known about the utility of various omega-3 fatty acid regimens, in particular fish oils, in preventing cardiac disease in ApoEKO mice. The purpose of this study was to determine the cardiovascular effects of omega-3 fatty acid supplementation with either safflower oil (control), fish oil, flaxseed oil, or designed oil in ApoEKO mice fed a high-fat diet for a total of 16 weeks. In-vivo cardiac function was assessed weekly using murine echocardiography. Blood pressure, plasma lipid levels, and brain natriuretic peptide (BNP) were serially measured. The results show that ApoEKO mice fed fish oil demonstrated an increase in left ventricular wall thickness as a result of increased afterload. Despite chronic treatment with fish oil over 16 weeks, blood pressure increased in ApoEKO mice by 20% compared with the baseline. Both echocardiographic evidence of left ventricular hypertrophy and biochemical increase in BNP levels confirmed diastolic dysfunction in ApoEKO mice fed fish oil. This suggests that high-fat diet supplemented with fish oil may lead to adverse cardiovascular effects in ApoE deficient mice.

Cigarette smoke-induced pulmonary inflammation is attenuated in CD69-deficient mice

2011 ◽  
Vol 31 (6) ◽  
pp. 434-439 ◽  
Author(s):  
Junichi Tsuyusaki ◽  
Fuminobu Kuroda ◽  
Yoshitoshi Kasuya ◽  
Shunsuke Ishizaki ◽  
Keita Yamauchi ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Pulmonary Inflammation ◽  
Deficient Mice

scholarly journals Cardiovascular Effects of PCB 126 (3,3’,4,4’,5-Pentachlorobiphenyl) in Zebrafish Embryos and Impact of Co-Exposure to Redox Modulating Chemicals

2019 ◽  
Vol 20 (5) ◽  
pp. 1065 ◽  
Author(s):  
Elisabet Teixidó ◽  
Marta Barenys ◽  
Ester Piqué ◽  
Joan Llobet ◽  
Jesús Gómez-Catalán
Keyword(s):  
Oxidative Stress ◽  
Developmental Toxicity ◽  
Environmental Pollutants ◽  
Cardiovascular Effects ◽  
Zebrafish Embryos ◽  
Oxidative Potential ◽  
Antioxidant Genes ◽  
Aryl Hydrocarbon ◽  
Low Concentrations ◽  
Pericardial Edema

The developing cardiovascular system of zebrafish is a sensitive target for many environmental pollutants, including dioxin-like compounds and pesticides. Some polychlorinated biphenyls (PCBs) can compromise the cardiovascular endothelial function by activating oxidative stress-sensitive signaling pathways. Therefore, we exposed zebrafish embryos to PCB126 or to several redox-modulating chemicals to study their ability to modulate the dysmorphogenesis produced by PCB126. PCB126 produced a concentration-dependent induction of pericardial edema and circulatory failure, and a concentration-dependent reduction of cardiac output and body length at 80 hours post fertilization (hpf). Among several modulators tested, the effects of PCB126 could be both positively and negatively modulated by different compounds; co-treatment with α-tocopherol (vitamin E liposoluble) prevented the adverse effects of PCB126 in pericardial edema, whereas co-treatment with sodium nitroprusside (a vasodilator compound) significantly worsened PCB126 effects. Gene expression analysis showed an up-regulation of cyp1a, hsp70, and gstp1, indicative of PCB126 interaction with the aryl hydrocarbon receptor (AhR), while the transcription of antioxidant genes (sod1, sod2; cat and gpx1a) was not affected. Further studies are necessary to understand the role of oxidative stress in the developmental toxicity of low concentrations of PCB126 (25 nM). Our results give insights into the use of zebrafish embryos for exploring mechanisms underlying the oxidative potential of environmental pollutants.

scholarly journals Nrf2-deficient mice are highly susceptible to cigarette smoke-induced emphysema

2005 ◽  
Vol 10 (12) ◽  
pp. 1113-1125 ◽  
Author(s):  
Takashi Iizuka ◽  
Yukio Ishii ◽  
Ken Itoh ◽  
Takumi Kiwamoto ◽  
Toru Kimura ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Deficient Mice

scholarly journals Cigarette Smoke-Induced Pulmonary Inflammation and Emphysema Are Attenuated in CCR6-Deficient Mice

2006 ◽  
Vol 177 (7) ◽  
pp. 4350-4359 ◽  
Author(s):  
Ken R. Bracke ◽  
An I. D’hulst ◽  
Tania Maes ◽  
Katrien B. Moerloose ◽  
Ingel K. Demedts ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Pulmonary Inflammation ◽  
Deficient Mice

scholarly journals Cigarette Smoke Exposure Promotes Arterial Thrombosis and Vessel Remodeling after Vascular Injury in Apolipoprotein E-Deficient Mice

2008 ◽  
Vol 45 (6) ◽  
pp. 480-492 ◽  
Author(s):  
Marco R. Schroeter ◽  
Matthias Sawalich ◽  
Tim Humboldt ◽  
Maren Leifheit ◽  
Kris Meurrens ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Cigarette Smoke ◽  
Vascular Injury ◽  
Arterial Thrombosis ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Vessel Remodeling ◽  
Deficient Mice

scholarly journals Cigarette smoke-induced iBALT mediates macrophage activation in a B cell-dependent manner in COPD

2014 ◽  
Vol 307 (9) ◽  
pp. L692-L706 ◽  
Author(s):  
Gerrit John-Schuster ◽  
Katrin Hager ◽  
Thomas M. Conlon ◽  
Martin Irmler ◽  
Johannes Beckers ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Cigarette Smoke ◽  
Macrophage Activation ◽  
Cell Function ◽  
Chronic Obstructive ◽  
Dependent Manner ◽  
Tissue Destruction ◽  
Deficient Mice

Chronic obstructive pulmonary disease (COPD) is characterized by a progressive decline in lung function, caused by exposure to exogenous particles, mainly cigarette smoke (CS). COPD is initiated and perpetuated by an abnormal CS-induced inflammatory response of the lungs, involving both innate and adaptive immunity. Specifically, B cells organized in iBALT structures and macrophages accumulate in the lungs and contribute to CS-induced emphysema, but the mechanisms thereof remain unclear. Here, we demonstrate that B cell-deficient mice are significantly protected against CS-induced emphysema. Chronic CS exposure led to an increased size and number of iBALT structures, and increased lung compliance and mean linear chord length in wild-type (WT) but not in B cell-deficient mice. The increased accumulation of lung resident macrophages around iBALT and in emphysematous alveolar areas in CS-exposed WT mice coincided with upregulated MMP12 expression. In vitro coculture experiments using B cells and macrophages demonstrated that B cell-derived IL-10 drives macrophage activation and MMP12 upregulation, which could be inhibited by an anti-IL-10 antibody. In summary, B cell function in iBALT formation seems necessary for macrophage activation and tissue destruction in CS-induced emphysema and possibly provides a new target for therapeutic intervention in COPD.

Sign in / Sign up

Export Citation Format

Share Document