Biomarker as a Research Tool in Linking Exposure to Air Particles and Respiratory Health

Suhaimi, Nur Faseeha; Jalaludin, Juliana

doi:10.1155/2015/962853

Cited by 31 publications

(31 citation statements)

References 56 publications

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“…The induction or exacerbation of airway inflammation is considered a common mechanism underlying the particle exposure-induced development of various adverse health effects in the respiratory and cardiovascular systems. [1][2][3][4][5][6] Thus, understanding how particulate matter triggers inflammatory reactions in the airway is a central issue in particle toxicology.…”

Section: Discussionmentioning

confidence: 99%

“…The pulmonary and cardiovascular effects of air pollution containing PM2.5 include impaired lung function; increased pathological incidence of chronic cough, bronchitis, and asthma; accelerated progression of atherosclerotic plaques; plaque instability; altered coagulation; venous thrombosis; and others. [1][2][3] Therefore, elucidating the toxicological mechanisms that link inhaled particles with damage to the respiratory and cardiovascular systems in vivo and in vitro is an active area of research.…”

Section: Introductionmentioning

confidence: 99%

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TP53-dependent autophagy links the ATR-CHEK1 axis activation to proinflammatory VEGFA production in human bronchial epithelial cells exposed to fine particulate matter (PM2.5)

Wang

et al. 2016

Autophagy

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Epidemiological and clinical studies have increasingly shown that fine particulate matter (PM2.5) is associated with a number of pathological respiratory diseases, such as bronchitis, asthma, and chronic obstructive pulmonary disease, which share the common feature of airway inflammation induced by particle exposure. Thus, understanding how PM2.5 triggers inflammatory responses in the respiratory system is crucial for the study of PM2.5 toxicity. In the current study, we found that exposing human bronchial epithelial cells (immortalized Beas-2B cells and primary cells) to PM2.5 collected in the winter in Wuhan, a city in southern China, induced a significant upregulation of VEGFA (vascular endothelial growth factor A) production, a signaling event that typically functions to control chronic airway inflammation and vascular remodeling. Further investigations showed that macroautophagy/autophagy was induced upon PM2.5 exposure and then mediated VEGFA upregulation by activating the SRC (SRC proto-oncogene, non-receptor tyrosine kinase)-STAT3 (signal transducer and activator of transcription 3) pathway in bronchial epithelial cells. By exploring the upstream signaling events responsible for autophagy induction, we revealed a requirement for TP53 (tumor protein p53) activation and the expression of its downstream target DRAM1 (DNA damage regulated autophagy modulator 1) for the induction of autophagy. These results thus extend the role of TP53-DRAM1-dependent autophagy beyond cell fate determination under genotoxic stress and to the control of proinflammatory cytokine production. Moreover, PM2.5 exposure strongly induced the activation of the ATR (ATR serine/threonine kinase)-CHEK1/CHK1 (checkpoint kinase 1) axis, which subsequently triggered TP53-dependent autophagy and VEGFA production in Beas-2B cells. Therefore, these findings suggest a novel link between processes regulating genomic integrity and airway inflammation via autophagy induction in bronchial epithelial cells under PM2.5 exposure.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

TP53-dependent autophagy links the ATR-CHEK1 axis activation to proinflammatory VEGFA production in human bronchial epithelial cells exposed to fine particulate matter (PM2.5)

Wang

et al. 2016

Autophagy

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“…An advantage of metabolomics involves the ability to detect substances derived from environmental exposures such as nutrition, for example tryptophan or essential fatty acids. Such nutrient‐derived markers might serve as markers of exposure [Suhaimi and Jalaludin, ] to exogenous environmental risk factors. Nutrients directly or indirectly interact with numerous non‐exposure biomarkers.…”

Section: Metabolomics Approaches To Biochemical Biomarker Discoverymentioning

confidence: 99%

Discovery of biochemical biomarkers for aggression: A role for metabolomics in psychiatry

Hagenbeek

Kluft

Hankemeier

et al. 2016

American J of Med Genetics Pt B

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Human aggression encompasses a wide range of behaviors and is related to many psychiatric disorders. We introduce the different classification systems of aggression and related disorders as a basis for discussing biochemical biomarkers and then present an overview of studies in humans (published between 1990 and 2015) that reported statistically significant associations of biochemical biomarkers with aggression, DSM-IV disorders involving aggression, and their subtypes. The markers are of different types, including inflammation markers, neurotransmitters, lipoproteins, and hormones from various classes. Most studies focused on only a limited portfolio of biomarkers, frequently a specific class only. When integrating the data, it is clear that compounds from several biological pathways have been found to be associated with aggressive behavior, indicating complexity and the need for a broad approach. In the second part of the paper, using examples from the aggression literature and psychiatric metabolomics studies, we argue that a better understanding of aggression would benefit from a more holistic approach such as provided by metabolomics. Key words: aggression; biomarkers; psychiatry; metabolomics INTRODUCTIONArguably, "violence and aggression are the most serious problems facing humanity" [Chichinadze et al., 2011]. One approach in the study of aggression and its etiology is at a biochemical level.Biochemical markers are intermediate to the outward phenotype and the underlying biology of aggression. They can aid in elucidating the causes and (patho) physiology of aggressive behavior [James et al., 2006;Scoriels et al., 2015]. One of the promises of 719Neuropsychiatric Genetics biochemical studies of central nervous system diseases is the development of biochemically based biomarkers [KaddurahDaouk and Krishnan, 2009]. Biomarkers can be applied in diagnosis, in assessment of disease stages, as indicators of disease prognosis, and for prediction or monitoring of interventions and treatment responses. Some biomarkers are "surrogate endpoints" which substitute clinical endpoints that reflect "how a patient feels, functions, or survives" [Atkinson et al., 2001]. There are several comprehensive overviews of biochemical compounds as potential biomarkers for aggression [e.g., Siever, 2008;Yanowitch and Coccaro, 2011], including reviews of neurotransmitters [e.g., de Almeida et al., 2005;Seo et al., 2008;Siever, 2008;Wallner and Machatschke, 2009;Chichinadze et al., 2011;Yanowitch and Coccaro, 2011;Haller, 2013;Umukoro et al., 2013;Morrison and Melloni, 2014;Narvaes and Almeida, 2014;Willner, 2015], hormonal networks [Simpson and Hons, 2001;Wingfield et al., 2006;Siever, 2008;Soma et al., 2008;Chichinadze et al., 2011;Eisenegger et al., 2011; Haller, 2014a,c;Soma et al., 2015], and cytokines [e.g., Zalcman and Siegel, 2006]. With a few exceptions [e.g., Siever, 2008], these reviews focus on a single biochemical class, studying biomarkers belonging to various different biochemical pathways in isolation. This makes it...

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“…Studies that investigated association between particulate pollution and health, reported that residents who resides near busy streets or those who use biomass fuel have increased risk of developing cardio pulmonary related illnesses (Clougherty, 2012;Wong et al, 2008;Davidson et al, 2005). This risk is attributed mainly to traffic movement and use of biomass fuel, which are the most activities reported to be the main contributors to particulate pollution, which is in agreement with findings from other studies conducted else were (Po et al, 2010;Torres-Duque et al, 2008;Wong et al, 2008;Davidson et al, 2005).…”

Section: Discussionsupporting

confidence: 75%

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IRJPEH

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Elsewhere, the risk of poor respiratory health outcomes due to particulate pollution among urban dwellers has been well documented. However, there is limited evidence to link urban air quality to population health among residents of Rehoboth metropolis, Namibians where the dominance of gravel roads in residential areas threaten dust pollution on daily basis. The study was conducted to establish the association between particulate pollution, house location and presence of gravel roads and the prevalence of selfreported respiratory ailments among residents of Rehoboth metropolis, Namibia. Data on residents' self-reported respiratory ailments, house location and environmental exposure were collected using structured questionnaires, while particulate dust levels were monitored using the ASTM D1739 reference method. The study found high particulate concentration and high self-reported respiratory ailments (> 66%) in Rehoboth metropolis. While respondents' location was associated with respiratory symptoms that include usual cough (p-value=0.009) and usual phlegm (p-value=0.04); distance of respondents' houses to gravel road location were not significantly associated with the self-reported respiratory ailments. However, high vehicle traffics on the gravel roads near homes was significantly associated with episode of cough, phlegm, and breathlessness (p-value=0.01). This study revealed that self-reported respiratory ailments, namely cough, phlegm and breathlessness are associated with high vehicle traffics on the gravel roads near homes. This may be due to increased dust pollution emanating from the high vehicle traffics on the gravel roads and suggests residents' allergic reactions to dust. Thus, it is recommended that as a short term mitigation measure, the town council should frequently sprinkle water on the gravel road to suppress dust emissions from vehicle traffics flow while long term control measure should include asphalting the road.

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Biomarker as a Research Tool in Linking Exposure to Air Particles and Respiratory Health

Cited by 31 publications

References 56 publications

TP53-dependent autophagy links the ATR-CHEK1 axis activation to proinflammatory VEGFA production in human bronchial epithelial cells exposed to fine particulate matter (PM2.5)

TP53-dependent autophagy links the ATR-CHEK1 axis activation to proinflammatory VEGFA production in human bronchial epithelial cells exposed to fine particulate matter (PM2.5)

Discovery of biochemical biomarkers for aggression: A role for metabolomics in psychiatry

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