Intra-city Differences in Cardiac Expression of Inflammatory Genes and Inflammasomes in Young Urbanites: A Pilot Study

Villarreal-Calderon, Rodolfo; Dale, Gary A.; Delgado‐Chávez, Ricardo; Torres‐Jardón, Ricardo; Zhu, Hongtu; Herritt, Lou; González-Maciel, Angélica; Reynoso-Robles, Rafael; Yuan, Ying; Wang, Jiaping; Solorio-López, Edelmira; Medina‐Cortina, Humberto; Calderón‐Garcidueñas, Lilian

doi:10.1293/tox.25.163

Cited by 16 publications

(26 citation statements)

References 63 publications

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“…Air pollution may up-regulate myocardial inflammatory genes and proteins in the RV (33). Although it is not feasible to study myocardial gene and protein profiles in such a large study of the general population, our findings remained after adjustment for C-reactive protein and interleukin-6 blood levels, which suggests that our findings were independent of systemic inflammation.…”

Section: Discussionmentioning

confidence: 63%

Traffic-related Air Pollution and the Right Ventricle. The Multi-ethnic Study of Atherosclerosis

Leary¹,

Kaufman²,

Barr

et al. 2014

Am J Respir Crit Care Med

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Rationale: Right heart failure is a cause of morbidity and mortality in common and rare heart and lung diseases. Exposure to traffic-related air pollution is linked to left ventricular hypertrophy, heart failure, and death. Relationships between traffic-related air pollution and right ventricular (RV) structure and function have not been studied.Objectives: To characterize the relationship between traffic-related air pollutants and RV structure and function.Methods: We included men and women with magnetic resonance imaging assessment of RV structure and function and estimated residential outdoor nitrogen dioxide (NO 2 ) concentrations from the Multi-ethnic Study of Atherosclerosis, a study of individuals free of clinical cardiovascular disease at baseline. Multivariable linear regression estimated associations between NO 2 exposure (averaged over the year prior to magnetic resonance imaging) and measures of RV structure and function after adjusting for demographics, anthropometrics, smoking status, diabetes mellitus, and hypertension. Adjustment for corresponding left ventricular parameters, traffic-related noise, markers of inflammation, and lung disease were considered in separate models. Secondary analyses considered oxides of nitrogen (NO x ) as the exposure. Measurements and Main Results:The study sample included 3,896 participants. In fully adjusted models, higher NO 2 was associated with greater RV mass and larger RV end-diastolic volume with or without further adjustment for corresponding left ventricular parameters, traffic-related noise, inflammatory markers, or lung disease (all P , 0.05). There was no association between NO 2 and RV ejection fraction. Relationships between NO x and RV morphology were similar.Conclusions: Higher levels of NO 2 exposure were associated with greater RV mass and larger RV end-diastolic volume.

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Section: Discussionmentioning

confidence: 63%

Traffic-related Air Pollution and the Right Ventricle. The Multi-ethnic Study of Atherosclerosis

Leary¹,

Kaufman²,

Barr

et al. 2014

Am J Respir Crit Care Med

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“…In contrast to the aforementioned data-mining study, a study of human autopsy ventricles from healthy young people who died in accidents revealed the expression of NLRC1, NLRP3 using RT-PCR, and detected 84 inflammasome signaling pathway genes using cDNA array analysis. More interestingly, significant upregulation of NLRC1, NLRP3 and of 29/84 inflammasome genes was found to be associated with air pollution (Villarreal-Calderon et al, 2012). …”

Section: Prrs In Cardiomyocytesmentioning

confidence: 99%

Innate immunity and cardiomyocytes in ischemic heart disease

Lin

Knowlton

2014

Life Sciences

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Myocardial ischemia/reperfusion (I/R) is the most common cause of myocardial inflammation, which is primarily a manifestation of the innate immune responses. Innate immunity is activated when pattern recognition receptors (PRRs) responds to molecular patterns common to microbes and to danger signals expressed by injured or infected cells, so called pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). The expression of various PRRs in cardiomyocytes and the release of DAMPs from cardiomyocytes subjected to I/R injury, through active mechanisms as well as passive processes, enable cardiomyocytes to generate innate immune responses. Studies in isolated heart and cardiomyocytes have confirmed the inflammatory and functional effects of cardiac PRRs especially toll-like receptors in response to I/R-derived DAMPs, such as heat shock proteins. This review addresses the active role of cardiomyocytes in mediating innate inflammatory responses to myocardial I/R. We propose that cardiomyocytes act as innate immune cells in myocardial I/R injury.

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“…Epidemiological studies reported that particulate air pollution not only has impact on the respiratory tract, but it has systemic and cardiovascular effects as well [1][2][3]. Acute exposure to particulate air pollution has been linked to a range of adverse cardiovascular events including hospital admissions with angina, myocardial infarction, and heart failure [4,5].…”

Section: Introductionmentioning

confidence: 99%

Diesel Exhaust Particles Induce Impairment of Vascular and Cardiac Homeostasis in Mice: Ameliorative Effect of Emodin

Dhaheri

Alamiri

Hefeiti

et al. 2015

Cell Physiol Biochem

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Background/Aim: There is strong epidemiological and clinical evidence that components of the cardiovascular system are adversely affected by particulate air pollutants through the generation of inflammation and oxidative stress. Emodin (1,3,8-trihydroxy-6-methylanthraquinone), which is commonly found in the roots of rhubarb plant, has strong antioxidant and anti-inflammatory effects. However, its possible protective effect on the cardiovascular effect of particulate air pollutants has never been reported before. Methods: We tested, in Tuck-Ordinary mice, the possible ameliorative effect of emodin on the acute (24h) cardiovascular effects of diesel exhaust particles (DEP, 1 mg/kg) or saline (control). Emodin (4 mg/kg) was administered intraperitoneally 1h before and 7h after pulmonary exposure to DEP. Twenty four h following DEP exposure, several cardiovascular endpoints were assessed. Results: Emodin significantly prevented the increase of leukocyte (n=8, P<0.001) and erythrocyte (n=8, P<0.01) numbers caused by DEP. Likewise, emodin abrogated DEP-induced increase of heart tissue levels of interleukin 1β (n=8, P<0.01) and tumour necrosis factor α (n=8, P<0.05), and significantly mitigated the change of the activities of antioxidant enzymes superoxide dismutase (n=8, P<0.001) and glutathione reductase (n=8, P<0.05). Emodin abolished the in vivo prothrombotic effect of DEP in pial arterioles (n=6, P<0.01) and venules (n=6, P<0.001). Similarly, emodin prevented platelet aggregation in vitro in whole blood (n=4-5, P<0.01), and the shortening of activated partial thromboplastin time (n=4, P<0.001) and prothrombin time (n=4, P<0.01) caused by DEP. Conclusion: We conclude that emodin treatment has consistently protected against DEP-induced impairment of vascular and cardiac homeostasis in mice. Our study provides experimental evidence that the use of functional food such as emodin, pending further studies, can be considered a useful agent and may have the potential to protect or mitigate the cardiovascular detrimental effects observed in people living in cities with high concentrations of particulate air pollution.

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Intra-city Differences in Cardiac Expression of Inflammatory Genes and Inflammasomes in Young Urbanites: A Pilot Study

Cited by 16 publications

References 63 publications

Traffic-related Air Pollution and the Right Ventricle. The Multi-ethnic Study of Atherosclerosis

Traffic-related Air Pollution and the Right Ventricle. The Multi-ethnic Study of Atherosclerosis

Innate immunity and cardiomyocytes in ischemic heart disease

Diesel Exhaust Particles Induce Impairment of Vascular and Cardiac Homeostasis in Mice: Ameliorative Effect of Emodin

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