Skip to main content
Key Specialties
Cardiology Diabetology Endocrinology Gastroenterology Geriatrics and Gerontology Gynecology and Obstetrics Hematology Infectious Disease Internal Medicine Nephrology Neurology Oncology Pediatrics Respiratory Medicine Rheumatology Surgery
Congress Coverage
2024 ACC Congress 2023 ESMO Congress 2023 EASD Congress 2023 ERS Congress 2023 ESC Congress 2023 EHA Congress 2023 ASCO Annual Meeting
Clinical Collections
Advances in Alzheimer’s

Keynote webinar | Spotlight on sleep in brain health

LIVE: Thursday 2nd May 2024, 18:00-19:30 (CEST)

Quality sleep is essential for health. But what happens to our brains when sleep patterns are disturbed? Join our experts to explore the interplay between sleep disruption and neurological diseases, and the questions that you need to be asking your patients to help you prevent the harmful effects of sleep deprivation.
ADVANCED SEARCH
Log in
Top
Cardiovascular Toxicology
Published in: Cardiovascular Toxicology 3/2019

01-06-2019 | Combustion

Combustion Particle-Induced Changes in Calcium Homeostasis: A Contributing Factor to Vascular Disease?

Authors: Jørn A. Holme, Bendik C. Brinchmann, Eric Le Ferrec, Dominique Lagadic-Gossmann, Johan Øvrevik

Published in: Cardiovascular Toxicology | Issue 3/2019

Login to get access

Abstract

Air pollution is the leading environmental risk factor for disease and premature death in the world. This is mainly due to exposure to urban air particle matter (PM), in particular, fine and ultrafine combustion-derived particles (CDP) from traffic-related air pollution. PM and CDP, including particles from diesel exhaust (DEP), and cigarette smoke have been linked to various cardiovascular diseases (CVDs) including atherosclerosis, but the underlying cellular mechanisms remain unclear. Moreover, CDP typically consist of carbon cores with a complex mixture of organic chemicals such as polycyclic aromatic hydrocarbons (PAHs) adhered. The relative contribution of the carbon core and adhered soluble components to cardiovascular effects of CDP is still a matter of discussion. In the present review, we summarize evidence showing that CDP affects intracellular calcium regulation, and argue that CDP-induced impairment of normal calcium control may be a critical cellular event through which CDP exposure contributes to development or exacerbation of cardiovascular disease. Furthermore, we highlight in vitro research suggesting that adhered organic chemicals such as PAHs may be key drivers of these responses. CDP, extractable organic material from CDP (CDP-EOM), and PAHs may increase intracellular calcium levels by interacting with calcium channels like transient receptor potential (TRP) channels, and receptors such as G protein-coupled receptors (GPCR; e.g., beta-adrenergic receptors [βAR] and protease-activated receptor 2 [PAR-2]) and the aryl hydrocarbon receptor (AhR). Clarifying a possible role of calcium signaling and mechanisms involved may increase our understanding of how air pollution contributes to CVD.
Literature
1.
WHO. (2016). Ambient air pollution: A global assesment of exposure and burden of disease. Geneva: World Health Organization.
2.
Siponen, T., Yli-Tuomi, T., Aurela, M., Dufva, H., Hillamo, R., Hirvonen, M. R., et al. (2015). Source-specific fine particulate air pollution and systemic inflammation in ischaemic heart disease patients. Occupational and Environmental Medicine, 72(4), 277–283.CrossRefPubMed
3.
Schneider, A., Neas, L. M., Graff, D. W., Herbst, M. C., Cascio, W. E., Schmitt, M. T., et al. (2010). Association of cardiac and vascular changes with ambient PM2.5 in diabetic individuals. Particle and Fibre Toxicology, 7, 14.CrossRefPubMedPubMedCentral
4.
Pope, C. A., Bhatnagar, A., McCracken, J. P., Abplanalp, W., Conklin, D. J., & O’Toole, T. (2016). Exposure to fine particulate air pollution is associated with endothelial injury and systemic inflammation. Circulation Research, 119(11), 1204–1214.CrossRefPubMedPubMedCentral
5.
Fariss, M. W., Gilmour, M. I., Reilly, C. A., Liedtke, W., & Ghio, A. J. (2013). Emerging mechanistic targets in lung injury induced by combustion-generated particles. Toxicological Science, 132(2), 253–267.CrossRef
6.
Cassee, F. R., Heroux, M. E., Gerlofs-Nijland, M. E., & Kelly, F. J. (2013). Particulate matter beyond mass: Recent health evidence on the role of fractions, chemical constituents and sources of emission. Inhalation Toxicology, 25(14), 802–812.CrossRefPubMedPubMedCentral
7.
Lewtas, J. (2007). Air pollution combustion emissions: Characterization of causative agents and mechanisms associated with cancer, reproductive, and cardiovascular effects. Mutation Research, 636(1–3), 95–133.CrossRefPubMed
8.
Kawasaki, S., Takizawa, H., Takami, K., Desaki, M., Okazaki, H., Kasama, T., et al. (2001). Benzene-extracted components are important for the major activity of diesel exhaust particles. American Journal of Respiratory Cell and Molecular Biology, 24, 419–426.CrossRefPubMed
9.
Bonvallot, V., Baeza-Squiban, A., Baulig, A., Brulant, S., Boland, S., Muzeau, F., et al. (2001). Organic compounds from diesel exhaust particles elicit a proinflammatory response in human airway epithelial cells and induce cytochrome p450 1A1 expression. American Journal of Respiratory Cell and Molecular Biology, 25, 515–521.CrossRefPubMed
10.
Totlandsdal, A. I., Herseth, J. I., Bolling, A. K., Kubatova, A., Braun, A., Cochran, R. E., et al. (2012). Differential effects of the particle core and organic extract of diesel exhaust particles. Toxicology Letters, 208(3), 262–268.CrossRefPubMed
11.
Ma, J. Y., & Ma, J. K. (2002). The dual effect of the particulate and organic components of diesel exhaust particles on the alteration of pulmonary immune/inflammatory responses and metabolic enzymes. Journal of Environmental Science Health Part C, 20(2), 117–147.CrossRef
12.
Keebaugh, A. J., Sioutas, C., Pakbin, P., Schauer, J. J., Mendez, L. B., & Kleinman, M. T. (2015). Is atherosclerotic disease associated with organic components of ambient fine particles? Science Total Environment, 533, 69–75.CrossRef
13.
Brinchmann, B. C., Le Ferrec, E., Podechard, N., Lagadic-Gossmann, D., Shoji, K. F., Penna, A., et al. (2018). Lipophilic chemicals from diesel exhaust particles trigger calcium response in human endothelial cells via aryl hydrocarbon receptor non-genomic signalling. International Journal of Molecular Science, 19(5), 1429.CrossRef
14.
Shapiro, D., Deering-Rice, C. E., Romero, E. G., Hughen, R. W., Light, A. R., Veranth, J. M., et al. (2013). Activation of transient receptor potential ankyrin-1 (TRPA1) in lung cells by wood smoke particulate material. Chemical Research in Toxicology, 26(5), 750–758.CrossRefPubMedPubMedCentral
15.
Mayati, A., Le Ferrec, E., Lagadic-Gossmann, D., & Fardel, O. (2012). Aryl hydrocarbon receptor-independent up-regulation of intracellular calcium concentration by environmental polycyclic aromatic hydrocarbons in human endothelial HMEC-1 cells. Environmental Toxicology, 27(9), 556–562.CrossRefPubMed
16.
McLaren, J. E., Michael, D. R., Ashlin, T. G., & Ramji, D. P. (2011). Cytokines, macrophage lipid metabolism and foam cells: Implications for cardiovascular disease therapy. Progress in Lipid Research, 50(4), 331–347.CrossRefPubMed
17.
Ramji, D. P., & Davies, T. S. (2015). Cytokines in atherosclerosis: Key players in all stages of disease and promising therapeutic targets. Cytokine & Growth Factor Reviews, 26(6), 673–685.CrossRef
18.
Donaldson, K., Stone, V., Borm, P. J. A., Jimenez, L. A., Gilmour, P. S., Schins, R. P. F., et al. (2003). Oxidative stress and calcium signaling in the adverse effects of environmental particles (PM10). Free Radical Biology & Medicine, 34(11), 1369–1382.CrossRef
19.
Donaldson, K., Stone, V., Seaton, A., & MacNee, W. (2001). Ambient particle inhalation and the cardiovascular system: Potential mechanisms. Environmental Health Perspectives, 109, 523–527.PubMedPubMedCentral
20.
de Kok, T. M., Driece, H. A., Hogervorst, J. G., & Briede, J. J. (2006). Toxicological assessment of ambient and traffic-related particulate matter: A review of recent studies. Mutation Research, 613(2–3), 103–122.CrossRefPubMed
21.
Maier, K. L., Alessandrini, F., Beck-Speier, I., Hofer, T. P., Diabate, S., Bitterle, E., et al. (2008). Health effects of ambient particulate matter–biological mechanisms and inflammatory responses to in vitro and in vivo particle exposures. Inhalation Toxicology, 20(3), 319–337.CrossRefPubMed
22.
Li, N., Hao, M., Phalen, R. F., Hinds, W. C., & Nel, A. E. (2003). Particulate air pollutants and asthma A paradigm for the role of oxidative stress in PM-induced adverse health effects. Clinical Immunology, 109, 250–265.CrossRefPubMed
23.
Sauer, H., Wartenberg, M., & Hescheler, J. (2001). Reactive oxygen species as intracellular messengers during cell growth and differentiation. Cellular Physiology and Biochemistry, 11, 173–186.CrossRefPubMed
24.
Ovrevik, J., Refsnes, M., Lag, M., Holme, J. A., & Schwarze, P. E. (2015). Activation of proinflammatory responses in cells of the airway mucosa by particulate matter: Oxidant- and non-oxidant-mediated triggering mechanisms. Biomolecules, 5(3), 1399–1440.CrossRefPubMedPubMedCentral
25.
Vogel, C. F. A., Sciullo, E., Wong, P., Kuzmicky, P., Kado, N., & Matsumura, F. (2005). Induction of proinflammatory cytokines and C-Reactive protein in human macrophage cell line U937 exposed to air pollution particulates. Environmental Health Perspectives, 113(11), 1536–1541.CrossRefPubMedPubMedCentral
26.
Mills, N. L., Tornqvist, H., Gonzalez, M. C., Vink, E., Robinson, S. D., Soderberg, S., et al. (2007). Ischemic and thrombotic effects of dilute diesel-exhaust inhalation in men with coronary heart disease. The New England journal of medicine, 357(11), 1075–1082.CrossRefPubMed
27.
Mills, N. L., Tornqvist, H., Robinson, S. D., Gonzalez, M., Darnley, K., MacNee, W., et al. (2005). Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis. Circulation, 112(25), 3930–3936.CrossRefPubMed
28.
Lucking, A. J., Lundback, M., Mills, N. L., Faratian, D., Barath, S. L., Pourazar, J., et al. (2008). Diesel exhaust inhalation increases thrombus formation in man. European Heart Journal, 29(24), 3043–3051.CrossRefPubMed
29.
Araujo, J. A., & Nel, A. E. (2009). Particulate matter and atherosclerosis: Role of particle size, composition and oxidative stress. Particle and Fibre Toxicology, 6, 24.CrossRefPubMedPubMedCentral
30.
Cohen, A. J., Brauer, M., Burnett, R., Anderson, H. R., Frostad, J., Estep, K., et al. (2017). Estimates and 25-year trends of the global burden of disease attributable to ambient air pollution: An analysis of data from the Global Burden of Diseases Study 2015. The Lancet, 389(10082), 1907–1918.CrossRef
31.
Brook, R. D., Rajagopalan, S., Pope, C. A., 3rd, Brook, J. R., Bhatnagar, A., Diez-Roux, A. V., et al. (2010). Particulate matter air pollution and cardiovascular disease: An update to the scientific statement from the American Heart Association. Circulation, 121(21), 2331–2378.CrossRefPubMed
32.
Perez, C. M., Hazari, M. S., & Farraj, A. K. (2015). Role of autonomic reflex arcs in cardiovascular responses to air pollution exposure. Cardiovascular Toxicology, 15(1), 69–78.CrossRefPubMedPubMedCentral
33.
Carll, A. P., Hazari, M. S., Perez, C. M., Krantz, Q. T., King, C. J., Winsett, D. W., et al. (2012). Whole and particle-free diesel exhausts differentially affect cardiac electrophysiology, blood pressure, and autonomic balance in heart failure-prone rats. Toxicological Sciences, 128(2), 490–499.CrossRefPubMedPubMedCentral
34.
Kodavanti, U. P. (2016). Stretching the stress boundary: Linking air pollution health effects to a neurohormonal stress response. Biochimica et Biophysica Acta, 1860(12), 2880–2890.CrossRefPubMed
35.
Hazari, M. S., Haykal-Coates, N., Winsett, D. W., Krantz, Q. T., King, C., Costa, D. L., et al. (2011). TRPA1 and sympathetic activation contribute to increased risk of triggered cardiac arrhythmias in hypertensive rats exposed to diesel exhaust. Environmental Health Perspectives, 119(7), 951–957.CrossRefPubMedPubMedCentral
36.
Araujo, J. A., Barajas, B., Kleinman, M., Wang, X., Bennett, B. J., Gong, K. W., et al. (2008). Ambient particulate pollutants in the ultrafine range promote early atherosclerosis and systemic oxidative stress. Circulation Research, 102(5), 589–596.CrossRefPubMedPubMedCentral
37.
Borm, P. J., Robbins, D., Haubold, S., Kuhlbusch, T., Fissan, H., Donaldson, K., et al. (2006). The potential risks of nanomaterials: A review carried out for ECETOC. Particle and Fibre Toxicology, 3, 11.CrossRefPubMedPubMedCentral
38.
Miller, M. R., Raftis, J. B., Langrish, J. P., McLean, S. G., Samutrtai, P., Connell, S. P., et al. (2017). Inhaled Nanoparticles accumulate at sites of vascular disease. ACS Nano, 11(5), 4542–4552.CrossRefPubMedPubMedCentral
39.
Miller, M. R., Raftis, J. B., Langrish, J. P., McLean, S. G., Samutrtai, P., Connell, S. P., et al. (2017). Correction to”Inhaled nanoparticles accumulate at sites of vascular disease”. ACS Nano, 11(10), 10623–10624.CrossRefPubMedPubMedCentral
40.
Penn, A., Murphy, G., Barker, S., Henk, W., & Penn, L. (2005). Combustion-derived ultrafine particles transport organic toxicants to target respiratory cells. Environmental Health Perspectives, 113(8), 956–963.CrossRefPubMedPubMedCentral
41.
Gerde, P., Muggenburg, B. A., Lundborg, M., & Dahl, A. R. (2001). The rapid alveolar absorption of diesel soot-adsorbed benzo[a]pyrene: Bioavailability, metabolism and dosimetry of an inhaled particle-borne carcinogen. Carcinogenesis, 22(5), 741–749.CrossRefPubMed
42.
Bostrom, C. E., Gerde, P., Hanberg, A., Jernstrom, B., Johansson, C., Kyrklund, T., et al. (2002). Cancer risk assessment, indicators, and guidelines for polycyclic aromatic hydrocarbons in the ambient air. Environmental Health Perspectives, 110(Suppl 3), 451–488.CrossRefPubMedPubMedCentral
43.
Zhang, Y. J., Weksler, B. B., Wang, L., Schwartz, J., & Santella, R. M. (1998). Immunohistochemical detection of polycyclic aromatic hydrocarbon-DNA damage in human blood vessels of smokers and non-smokers. Atherosclerosis, 140(2), 325–331.CrossRefPubMed
44.
Korashy, H. M., & El-Kadi, A. O. S. (2008). The role of aryl hydrocarbon receptor in the pathogenesis of cardiovascular diseases. Drug Metabolism Reviews, 38(3), 411–450.CrossRef
45.
Brinchmann, B. C., Skuland, T., Rambol, M. H., Szoke, K., Brinchmann, J. E., Gutleb, A. C., et al. (2018). Lipophilic components of diesel exhaust particles induce pro-inflammatory responses in human endothelial cells through AhR dependent pathway(s). Particle and Fibre Toxicology, 15(1), 21.CrossRefPubMedPubMedCentral
46.
Klein, S. G., Cambier, S., Hennen, J., Legay, S., Serchi, T., Nelissen, I., et al. (2017). Endothelial responses of the alveolar barrier in vitro in a dose-controlled exposure to diesel exhaust particulate matter. Particle and Fibre Toxicology, 14(1), 7.CrossRefPubMedPubMedCentral
47.
Forchhammer, L., Loft, S., Roursgaard, M., Cao, Y., Riddervold, I. S., Sigsgaard, T., et al. (2012). Expression of adhesion molecules, monocyte interactions and oxidative stress in human endothelial cells exposed to wood smoke and diesel exhaust particulate matter. Toxicology Letters, 209(2), 121–128.CrossRefPubMed
48.
Lawal, A. O., Zhang, M., Dittmar, M., Lulla, A., & Araujo, J. A. (2015). Heme oxygenase-1 protects endothelial cells from the toxicity of air pollutant chemicals. Toxicology and Applied Pharmacology, 284(3), 281–291.CrossRefPubMedPubMedCentral
49.
Cao, Y., Long, J., Ji, Y., Chen, G., Shen, Y., Gong, Y., et al. (2016). Foam cell formation by particulate matter (PM) exposure: A review. Inhalation Toxicology, 28(13), 583–590.CrossRefPubMed
50.
Krishnan, R. M., Adar, S. D., Szpiro, A. A., Jorgensen, N. W., Van Hee, V. C., Barr, R. G., et al. (2012). Vascular responses to long- and short-term exposure to fine particulate matter: MESA Air (Multi-Ethnic Study of Atherosclerosis and Air Pollution). Journal of the American College of Cardiology, 60(21), 2158–2166.CrossRefPubMedPubMedCentral
51.
Van Eeden, S., Leipsic, J., Paul Man, S. F., & Sin, D. D. (2012). The relationship between lung inflammation and cardiovascular disease. American Journal of Respiratory and Critical Care Medicine, 186(1), 11–16.CrossRefPubMed
52.
Brauner, E. V., Forchhammer, L., Moller, P., Simonsen, J., Glasius, M., Wahlin, P., et al. (2007). Exposure to ultrafine particles from ambient air and oxidative stress-induced DNA damage. Environmental Health Perspectives, 115(8), 1177–1182.CrossRefPubMedPubMedCentral
53.
Sorensen, M., Daneshvar, B., Hansen, M., Dragsted, L. O., Hertel, O., Knudsen, L., et al. (2003). Personal PM2.5 exposure and markers of oxidative stress in blood. Environmental Health Perspectives, 111(2), 161–166.CrossRefPubMedPubMedCentral
54.
Moller, P., Christophersen, D. V., Jacobsen, N. R., Skovmand, A., Gouveia, A. C., Andersen, M. H., et al. (2016). Atherosclerosis and vasomotor dysfunction in arteries of animals after exposure to combustion-derived particulate matter or nanomaterials. Critical Reviews in Toxicology, 46(5), 437–476.CrossRefPubMed
55.
56.
Conway, J. D., Bartolotta, T., Abdullah, L. H., & Davis, C. W. (2003). Regulation of mucin secretion from human bronchial epithelial cells grown in murine hosted xenografts. American Journal of Physiology. Lung Cellular and Molecular Physiology, 284(6), L945–954.CrossRefPubMed
57.
Haller, T., Ortmayr, J., Friedrich, F., Volkl, H., & Dietl, P. (1998). Dynamics of surfactant release in alveolar type II cells. Proceedings of the National academy of Sciences of the United States of America, 95(4), 1579–1584.CrossRefPubMedPubMedCentral
58.
Lansley, A. B., & Sanderson, M. J. (1999). Regulation of airway ciliary activity by Ca2+ : Simultaneous measurement of beat frequency and intracellular Ca2+. Biophysical Journal, 77(1), 629–638.CrossRefPubMedPubMedCentral
59.
Racioppi, L., & Means, A. R. (2012). Calcium/calmodulin-dependent protein kinase kinase 2: Roles in signaling and pathophysiology. Journal of Biological Chemistry, 287(38), 31658–31665.CrossRefPubMedPubMedCentral
60.
61.
Yao, X., & Garland, C. J. (2005). Recent developments in vascular endothelial cell transient receptor potential channels. Circulation Research, 97(9), 853–863.CrossRefPubMed
62.
Sandow, S. L., Senadheera, S., Grayson, T. H., Welsh, D. G., & Murphy, T. V. (2012). Calcium and endothelium-mediated vasodilator signaling. Advances in Experimental Medicine and Biology, 740, 811–831.CrossRefPubMed
63.
Sandow, S. L., Haddock, R. E., Hill, C. E., Chadha, P. S., Kerr, P. M., Welsh, D. G., et al. (2009). What’s where and why at a vascular myoendothelial microdomain signalling complex. Clinical and Experimental Pharmacology and Physiology, 36(1), 67–76.CrossRefPubMed
64.
Bagher, P., & Segal, S. S. (2011). Regulation of blood flow in the microcirculation: Role of conducted vasodilation. Acta physiologica (Oxford, England), 202(3), 271–284.CrossRefPubMedCentral
65.
Straub, A. C., Zeigler, A. C., & Isakson, B. E. (2014). The myoendothelial junction: connections that deliver the message. Physiology (Bethesda), 29(4), 242–249.
66.
Tiruppathi, C., Minshall, R. D., Paria, B. C., Vogel, S. M., & Malik, A. B. (2002). Role of Ca2 + signaling in the regulation of endothelial permeability. Vascular Pharmacology, 39(4–5), 173–185.CrossRefPubMed
67.
Tiruppathi, C., Ahmmed, G. U., Vogel, S. M., & Malik, A. B. (2006). Ca2 + signaling, TRP channels, and endothelial permeability. Microcirculation, 13(8), 693–708.CrossRefPubMed
68.
Barbado, M., Fablet, K., Ronjat, M., & De Waard, M. (2009). Gene regulation by voltage-dependent calcium channels. Biochimica et Biophysica Acta (BBA)-Molecular Cell Research, 1793(6), 1096–1104.CrossRef
69.
Goswami, R., Merth, M., Sharma, S., Alharbi, M. O., Aranda-Espinoza, H., Zhu, X., et al. (2017). TRPV4 calcium-permeable channel is a novel regulator of oxidized LDL-induced macrophage foam cell formation. Free Radical Biology and Medicine, 110, 142–150.CrossRefPubMed
70.
Mendes-Silverio, C. B., Alexandre, E. M., Lescano, C. H., Antunes, E., & Monica, F. Z. (2018). Mirabegron, a beta3-adrenoceptor agonist reduced platelet aggregation through cyclic adenosine monophosphate accumulation. European Journal of Pharmacology, 829, 79–84.CrossRefPubMed
71.
Neri, T., Pergoli, L., Petrini, S., Gravendonk, L., Balia, C., Scalise, V., et al. (2016). Particulate matter induces prothrombotic microparticle shedding by human mononuclear and endothelial cells. Toxicology in Vitro, 32, 333–338.CrossRefPubMed
72.
Ramsey, I. S., Delling, M., & Clapham, D. E. (2006). An introduction to TRP channels. Annual Review of Physiology, 68, 619–647.CrossRefPubMed
73.
Caterina, M. J., & Julius, D. (2001). The vanilloid receptor: a molecular gateway to the pain pathway. Annual Review of Neuroscience, 24, 487–517.CrossRefPubMed
74.
Chakraborty, S., & Hasan, G. (2012). IP3R, store-operated Ca2+ entry and neuronal Ca2+ homoeostasis in Drosophila. Biochemical Society Transactions, 40(1), 279–281.CrossRefPubMed
75.
Liao, Y., Erxleben, C., Abramowitz, J., Flockerzi, V., Zhu, M. X., Armstrong, D. L., et al. (2008). Functional interactions among Orai1, TRPCs, and STIM1 suggest a STIM-regulated heteromeric Orai/TRPC model for SOCE/Icrac channels. Proceedings of the National academy of Sciences of the United States of America, 105(8), 2895–2900.CrossRefPubMedPubMedCentral
76.
Ong, H. L., & Ambudkar, I. S. (2017). STIM-TRP Pathways and Microdomain Organization: Contribution of TRPC1 in Store-Operated Ca(2 +) Entry: Impact on Ca(2 +) Signaling and Cell Function. Advances in Experimental Medicine and Biology, 993, 159–188.CrossRefPubMed
77.
Altier, C. (2012). GPCR and voltage-gated calcium channels (VGCC) signaling complexes. Sub-cellular Biochemistry, 63, 241–262.CrossRefPubMed
78.
Zamponi, G. W. (2015). Calcium channel signaling complexes with receptors and channels. Current Molecular Pharmacology, 8(1), 8–11.CrossRefPubMed
79.
Bylund, D. B., Eikenberg, D. C., Hieble, J. P., Langer, S. Z., Lefkowitz, R. J., Minneman, K. P., et al. (1994). International Union of Pharmacology nomenclature of adrenoceptors. Pharmacological Reviews, 46(2), 121–136.PubMed
80.
Lowell, B. B., & Flier, J. S. (1997). Brown adipose tissue, beta 3-adrenergic receptors, and obesity. Annual Review of Medicine, 48, 307–316.CrossRefPubMed
81.
Hirano, K. (2007). The roles of proteinase-activated receptors in the vascular physiology and pathophysiology. Arteriosclerosis, Thrombosis, and Vascular Biology, 27(1), 27–36.CrossRefPubMed
82.
Alberelli, M. A., & De Candia, E. (2014). Functional role of protease activated receptors in vascular biology. Vascular Pharmacology, 62(2), 72–81.CrossRefPubMed
83.
Esser, C., & Rannug, A. (2015). The aryl hydrocarbon receptor in barrier organ physiology, immunology, and toxicology. Pharmacological Reviews, 67(2), 259–279.CrossRefPubMed
84.
Barouki, R., Aggerbeck, M., Aggerbeck, L., & Coumoul, X. (2012). The aryl hydrocarbon receptor system. Drug Metabolism and Drug Interactions, 27(1), 3–8.CrossRefPubMed
85.
Tian, Y., Rabson, A. B., & Gallo, M. A. (2002). Ah receptor and NF-kappaB interactions: Mechanisms and physiological implications. Chemico-Biological Interactions, 141(1–2), 97–115.CrossRefPubMed
86.
Vogel, C. F., & Matsumura, F. (2009). A new cross-talk between the aryl hydrocarbon receptor and RelB, a member of the NF-kappaB family. Biochemical Pharmacology, 77(4), 734–745.CrossRefPubMed
87.
Denison, M. S., Soshilov, A. A., He, G., DeGroot, D. E., & Zhao, B. (2011). Exactly the same but different: Promiscuity and diversity in the molecular mechanisms of action of the aryl hydrocarbon (dioxin) receptor. Toxicological Sciences, 124(1), 1–22.CrossRefPubMedPubMedCentral
88.
Guyot, E., Chevallier, A., Barouki, R., & Coumoul, X. (2013). The AhR twist: Ligand-dependent AhR signaling and pharmaco-toxicological implications. Drug Discovery Today, 18(9–10), 479–486.CrossRefPubMed
89.
Matsumura, F. (2009). The significance of the nongenomic pathway in mediating inflammatory signaling of the dioxin-activated Ah receptor to cause toxic effects. Biochemical Pharmacology, 77(4), 608–626.CrossRefPubMed
90.
Tomkiewicz, C., Herry, L., Bui, L. C., Metayer, C., Bourdeloux, M., Barouki, R., et al. (2013). The aryl hydrocarbon receptor regulates focal adhesion sites through a non-genomic FAK/Src pathway. Oncogene, 32(14), 1811–1820.CrossRefPubMed
91.
N’Diaye, M., Le Ferrec, E., Lagadic-Gossmann, D., Corre, S., Gilot, D., Lecureur, V., et al. (2006). Aryl hydrocarbon receptor- and calcium-dependent induction of the chemokine CCL1 by the environmental contaminant benzo[a]pyrene. Journal of Biological Chemistry, 281(29), 19906–19915.CrossRefPubMed
92.
Monteiro, P., Gilot, D., Le Ferrec, E., Rauch, C., Lagadic-Gossmann, D., & Fardel, O. (2008). Dioxin-mediated up-regulation of aryl hydrocarbon receptor target genes is dependent on the calcium/calmodulin/CaMKIalpha pathway. Molecular Pharmacology, 73(3), 769–777.CrossRefPubMed
93.
Nicolson, G. L. (2014). The Fluid-Mosaic Model of Membrane Structure: Still relevant to understanding the structure, function and dynamics of biological membranes after more than 40 years. Biochimica et Biophysica Acta, 1838(6), 1451–1466.CrossRefPubMed
94.
Bastiani, M., & Parton, R. G. (2010). Caveolae at a glance. Journal of Cell Science, 123(Pt 22), 3831–3836.CrossRefPubMed
95.
van Deurs, B., Roepstorff, K., Hommelgaard, A. M., & Sandvig, K. (2003). Caveolae: Anchored, multifunctional platforms in the lipid ocean. Trends in Cell Biology, 13(2), 92–100.CrossRefPubMed
96.
Santos, A. L., & Preta, G. (2018). Lipids in the cell: Organisation regulates function. Cellular and Molecular Life Sciences, 75, 1909–1927.CrossRefPubMed
97.
Patel, H. H., Murray, F., & Insel, P. A. (2008). Caveolae as organizers of pharmacologically relevant signal transduction molecules. Annual Review of Pharmacology and Toxicology, 48, 359–391.CrossRefPubMedPubMedCentral
98.
Isshiki, M., & Anderson, R. G. (1999). Calcium signal transduction from caveolae. Cell Calcium, 26(5), 201–208.CrossRefPubMed
99.
100.
Majkova, Z., Toborek, M., & Hennig, B. (2010). The role of caveolae in endothelial cell dysfunction with a focus on nutrition and environmental toxicants. Journal of Cellular and Molecular Medicine, 14(10), 2359–2370.CrossRefPubMedPubMedCentral
101.
Saini, H. K., Arneja, A. S., & Dhalla, N. S. (2004). Role of cholesterol in cardiovascular dysfunction. Canadian Journal of Cardiology, 20(3), 333–346.PubMed
102.
Podechard, N., Chevanne, M., Fernier, M., Tete, A., Collin, A., Cassio, D., et al. (2016). Zebrafish larva as a reliable model for in vivo assessment of membrane remodeling involvement in the hepatotoxicity of chemical agents. Journal of Applied Toxicology, 37, 732–746.CrossRefPubMed
103.
Tekpli, X., Holme, J. A., Sergent, O., & Lagadic-Gossmann, D. (2011). Importance of plasma membrane dynamics in chemical-induced carcinogenesis. Recent Patents on Anti-Cancer Drug Discovery, 6(3), 347–353.CrossRefPubMed
104.
Brinchmann, B. C., Ferrec, E. L., Bisson, W. H., Podechard, N., Huitfeldt, H. S., Gallais, I., et al. (2018). Evidence of selective activation of aryl hydrocarbon receptor nongenomic calcium signaling by pyrene. Biochemical Pharmacology, 158, 1–12.CrossRefPubMed
105.
Li, J., Kanju, P., Patterson, M., Chew, W. L., Cho, S. H., Gilmour, I., et al. (2011). TRPV4-mediated calcium influx into human bronchial epithelia upon exposure to diesel exhaust particles. Environmental Health Perspectives, 119(6), 784–793.CrossRefPubMedPubMedCentral
106.
Mayati, A., Levoin, N., Paris, H., N’Diaye, M., Courtois, A., Uriac, P., et al. (2012). Induction of intracellular calcium concentration by environmental benzo(a)pyrene involves a beta2-adrenergic receptor/adenylyl cyclase/Epac-1/inositol 1,4,5-trisphosphate pathway in endothelial cells. Journal of Biological Chemistry, 287(6), 4041–4052.CrossRefPubMed
107.
Mayati, A., Le Ferrec, E., Holme, J. A., Fardel, O., Lagadic-Gossmann, D., & Ovrevik, J. (2014). Calcium signaling and beta2-adrenergic receptors regulate 1-nitropyrene induced CXCL8 responses in BEAS-2B cells. Toxicology in Vitro, 28(6), 1153–1157.CrossRefPubMed
108.
Deering-Rice, C. E., Romero, E. G., Shapiro, D., Hughen, R. W., Light, A. R., Yost, G. S., et al. (2011). Electrophilic components of diesel exhaust particles (DEP) activate transient receptor potential ankyrin-1 (TRPA1): A probable mechanism of acute pulmonary toxicity for DEP. Chemical Research in Toxicology, 24(6), 950–959.CrossRefPubMedPubMedCentral
109.
Roveri, A., Coassin, M., Maiorino, M., Zamburlini, A., van Amsterdam, F. T., Ratti, E., et al. (1992). Effect of hydrogen peroxide on calcium homeostasis in smooth muscle cells. Archives of Biochemistry and Biophysics, 297(2), 265–270.CrossRefPubMed
110.
Robison, T. W., Zhou, H., & Forman, H. J. (1995). Modulation of ADP-stimulated inositol phosphate metabolism in rat alveolar macrophages by oxidative stress. Archives of Biochemistry and Biophysics, 318(1), 215–220.CrossRefPubMed
111.
Fusi, F., Saponara, S., Gagov, H., & Sgaragli, G. (2001). 2,5-Di-t-butyl-1,4-benzohydroquinone (BHQ) inhibits vascular L-type Ca(2 +) channel via superoxide anion generation. British Journal of Pharmacology, 133(7), 988–996.CrossRefPubMedPubMedCentral
112.
Deering-Rice, C. E., Johansen, M. E., Roberts, J. K., Thomas, K. C., Romero, E. G., Lee, J., et al. (2012). Transient receptor potential vanilloid-1 (TRPV1) is a mediator of lung toxicity for coal fly ash particulate material. Molecular Pharmacology, 81(3), 411–419.CrossRefPubMedPubMedCentral
113.
Li, Jinju, Kanju, Patrick, Patterson, Michael, Chew, Wei-Leong, Cho, Seung-Hyun, Gilmour, Ian, et al. (2011). TRPV4-mediated calcium influx into human bronchial epithelia upon exposure to diesel exhaust particles. Environmental Health Perspectives, 119, 784–793.CrossRefPubMedPubMedCentral
114.
Barath, S., Mills, N. L., Lundback, M., Tornqvist, H., Lucking, A. J., Langrish, J. P., et al. (2010). Impaired vascular function after exposure to diesel exhaust generated at urban transient running conditions. Particle and Fibre Toxicology, 7, 19.CrossRefPubMedPubMedCentral
115.
Chen, Q., Guo, F., Liu, S., Xiao, J., Wang, C., Snowise, S., et al. (2012). Calcium channel blockers prevent endothelial cell activation in response to necrotic trophoblast debris: Possible relevance to pre-eclampsia. Cardiovascular Research, 96(3), 484–493.CrossRefPubMed
116.
Smedlund, K., Bah, M., & Vazquez, G. (2012). On the role of endothelial TRPC3 channels in endothelial dysfunction and cardiovascular disease. Cardiovascular & Hematological Agents in Medicinal Chemistry, 10(3), 265–274.CrossRef
117.
Abramowitz, J., & Birnbaumer, L. (2009). Physiology and pathophysiology of canonical transient receptor potential channels. The Faseb Journal, 23(2), 297–328.CrossRefPubMedPubMedCentral
118.
Dietrich, A., Kalwa, H., Fuchs, B., Grimminger, F., Weissmann, N., & Gudermann, T. (2007). In vivo TRPC functions in the cardiopulmonary vasculature. Cell Calcium, 42(2), 233–244.CrossRefPubMed
119.
120.
Sullivan, M. N., & Earley, S. (2013). TRP channel Ca(2 +) sparklets: Fundamental signals underlying endothelium-dependent hyperpolarization. American Journal of Physiology. Cell Physiology, 305(10), C999–c1008.CrossRefPubMedPubMedCentral
121.
122.
Liu, D. Y., Thilo, F., Scholze, A., Wittstock, A., Zhao, Z. G., Harteneck, C., et al. (2007). Increased store-operated and 1-oleoyl-2-acetyl-sn-glycerol-induced calcium influx in monocytes is mediated by transient receptor potential canonical channels in human essential hypertension. Journal of Hypertension, 25(4), 799–808.CrossRefPubMed
123.
Liu, D. Y., Scholze, A., Kreutz, R., Wehland-von-Trebra, M., Zidek, W., Zhu, Z. M., et al. (2007). Monocytes from spontaneously hypertensive rats show increased store-operated and second messenger-operated calcium influx mediated by transient receptor potential canonical Type 3 channels. American Journal of Hypertension, 20(10), 1111–1118.CrossRefPubMed
124.
De Backer, G. (2003). European guidelines on cardiovascular disease prevention in clinical practice Third Joint Task Force of European and other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of eight societies and by invited experts). European Heart Journal, 24(17), 1601–1610.CrossRefPubMed
125.
Kolmus, K., Tavernier, J., & Gerlo, S. (2015). beta2-Adrenergic receptors in immunity and inflammation: Stressing NF-kappaB. Brain, Behavior, and Immunity, 45, 297–310.CrossRefPubMed
126.
Wachter, S. B., & Gilbert, E. M. (2012). Beta-adrenergic receptors, from their discovery and characterization through their manipulation to beneficial clinical application. Cardiology, 122(2), 104–112.CrossRefPubMed
127.
Mayati, A., Podechard, N., Rineau, M., Sparfel, L., Lagadic-Gossmann, D., Fardel, O., et al. (2017). Benzo(a)pyrene triggers desensitization of beta2-adrenergic pathway. Scientific Reports, 7(1), 3262.CrossRefPubMedPubMedCentral
128.
Ovrevik, J., Refsnes, M., Totlandsdal, A. I., Holme, J. A., Schwarze, P. E., & Lag, M. (2011). TACE/TGF-alpha/EGFR regulates CXCL8 in bronchial epithelial cells exposed to particulate matter components. European Respiratory Journal, 38(5), 1189–1199.CrossRefPubMed
129.
Li, J., Ghio, A. J., Cho, S.-H., Brinckerhoff, C. E., Simon, S. A., & Liedtke, W. (2009). Diesel exhaust particles activate the matrix-metalloproteinase-1 gene in human bronchial epithelia in a β-arrestin–dependent manner via activation of RAS. Environmental Health Perspectives, 117(3), 400–409.CrossRefPubMed
130.
Bach, N., Bolling, A. K., Brinchmann, B. C., Totlandsdal, A. I., Skuland, T., Holme, J. A., et al. (2015). Cytokine responses induced by diesel exhaust particles are suppressed by PAR-2 silencing and antioxidant treatment, and driven by polar and non-polar soluble constituents. Toxicology Letters, 238(2), 72–82.CrossRefPubMed
131.
Brinchmann, B. C., Le Ferrec, E., Podechard, N., Lagadic-Gossmann, D., Holme, J. A., & Ovrevik, J. (2018). Organic chemicals from diesel exhaust particles affects intracellular calcium, inflammation and beta-adrenoceptors in endothelial cells. Toxicology Letters, 302, 18–27.CrossRefPubMed
132.
Puga, A. (1997). Sustained increase in intracellular free calcium and activation of cyclooxygenase-2 expression in mouse hepatoma cells treated with Dioxin. Biochemical Pharmacology, 54, 1287–1296.CrossRefPubMed
133.
Karras, J. G., Morris, D. L., Matulka, R. A., Kramer, C. M., & Holsapple, M. P. (1996). 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) elevates basal B-cell intracellular calcium concentration and suppresses surface Ig- but not CD40-induced antibody secretion. Toxicology and Applied Pharmacology, 137(2), 275–284.CrossRefPubMed
134.
Morales-Hernandez, A., Sanchez-Martin, F. J., Hortigon-Vinagre, M. P., Henao, F., & Merino, J. M. (2012). 2,3,7,8-Tetrachlorodibenzo-p-dioxin induces apoptosis by disruption of intracellular calcium homeostasis in human neuronal cell line SHSY5Y. Apoptosis: An International Journal on Programmed Cell Death, 17(11), 1170–1181.CrossRef
135.
Nguyen, L. P., & Bradfield, C. A. (2008). The search for endogenous activators of the aryl hydrocarbon receptor. Chemical Research in Toxicology, 21(1), 102–116.CrossRefPubMed
136.
Savouret, J. F., Berdeaux, A., & Casper, R. F. (2003). The aryl hydrocarbon receptor and its xenobiotic ligands: A fundamental trigger for cardiovascular diseases. Nutrition, Metabolism, and Cardiovascular Diseases: NMCD, 13(2), 104–113.CrossRefPubMed
137.
Vogel, C. F., Sciullo, E., & Matsumura, F. (2004). Activation of inflammatory mediators and potential role of ah-receptor ligands in foam cell formation. Cardiovascular Toxicology, 4(4), 363–373.CrossRefPubMed
138.
Wu, D., Nishimura, N., Kuo, V., Fiehn, O., Shahbaz, S., Van Winkle, L., et al. (2011). Activation of aryl hydrocarbon receptor induces vascular inflammation and promotes atherosclerosis in apolipoprotein E-/- mice. Arteriosclerosis, Thrombosis, and Vascular Biology, 31(6), 1260–1267.CrossRefPubMedPubMedCentral
139.
Sciullo, E. M., Vogel, C. F., Li, W., & Matsumura, F. (2008). Initial and extended inflammatory messages of the nongenomic signaling pathway of the TCDD-activated Ah receptor in U937 macrophages. Archives of Biochemistry and Biophysics, 480(2), 143–155.CrossRefPubMed
140.
Hanneman, W. H., Legare, M., Barhoumi, R., Burghardt, R., Safe, S., & Tiffany-Castiglioni, E. (1996). Stimulation of calcium uptake in cultured rat hippocampal neurons by 2,3,7,8-tetrachlorodibenzo-p-dioxin. Toxicology, 112(1), 19–28.CrossRefPubMed
141.
Su, H. H., Lin, H. T., Suen, J. L., Sheu, C. C., Yokoyama, K. K., Huang, S. K., et al. (2016). Aryl hydrocarbon receptor-ligand axis mediates pulmonary fibroblast migration and differentiation through increased arachidonic acid metabolism. Toxicology, 370, 116–126.CrossRefPubMed
142.
Maaetoft-Udsen, K., Shimoda, L. M., Frokiaer, H., & Turner, H. (2012). Aryl hydrocarbon receptor ligand effects in RBL2H3 cells. Journal of Immunotoxicology, 9(3), 327–337.CrossRefPubMedPubMedCentral
143.
Rainville, J., Pollard, K., & Vasudevan, N. (2015). Membrane-initiated non-genomic signaling by estrogens in the hypothalamus: Cross-talk with glucocorticoids with implications for behavior. Frontiers in Endocrinology, 6, 18.CrossRefPubMedPubMedCentral
144.
Foradori, C. D., Weiser, M. J., & Handa, R. J. (2008). Non-genomic actions of androgens. Frontiers in Neuroendocrinology, 29(2), 169–181.CrossRefPubMed
145.
Ropero, A. B., Juan-Pico, P., Rafacho, A., Fuentes, E., Bermudez-Silva, F. J., Roche, E., et al. (2009). Rapid non-genomic regulation of Ca2+ signals and insulin secretion by PPAR alpha ligands in mouse pancreatic islets of Langerhans. Journal of Endocrinology, 200(2), 127–138.CrossRefPubMed
146.
Meyer, M. R., Haas, E., Prossnitz, E. R., & Barton, M. (2009). Non-genomic regulation of vascular cell function and growth by estrogen. Molecular and Cellular Endocrinology, 308(1–2), 9–16.CrossRefPubMedPubMedCentral
147.
Kim, K. H., & Bender, J. R. (2009). Membrane-initiated actions of estrogen on the endothelium. Molecular and Cellular Endocrinology, 308(1–2), 3–8.CrossRefPubMedPubMedCentral
148.
Moriarty, K., Kim, K. H., & Bender, J. R. (2006). Minireview: Estrogen receptor-mediated rapid signaling. Endocrinology, 147(12), 5557–5563.CrossRefPubMed
149.
Chambliss, K. L., Yuhanna, I. S., Anderson, R. G., Mendelsohn, M. E., & Shaul, P. W. (2002). ERbeta has nongenomic action in caveolae. Molecular Endocrinology (Baltimore, Md), 16(5), 938–946.
150.
Rey-Barroso, J. (2014). The Dioxin receptor modulates Caveolin-1 mobilization during directional migration: Role of cholesterol. Cell Communication and Signaling, 12, 57.CrossRefPubMedPubMedCentral
151.
Dong, B., & Matsumura, F. (2008). Roles of cytosolic phospholipase A2 and Src kinase in the early action of 2,3,7,8-tetrachlorodibenzo-p-dioxin through a nongenomic pathway in MCF10A cells. Molecular Pharmacology, 74(1), 255–263.CrossRefPubMed
152.
Graziani, A., Bricko, V., Carmignani, M., Graier, W. F., & Groschner, K. (2004). Cholesterol- and caveolin-rich membrane domains are essential for phospholipase A2-dependent EDHF formation. Cardiovascular Research, 64(2), 234–242.CrossRefPubMed
153.
Murata, M., Peranen, J., Schreiner, R., Wieland, F., Kurzchalia, T. V., & Simons, K. (1995). VIP21/caveolin is a cholesterol-binding protein. Proceedings of the National academy of Sciences of the United States of America, 92(22), 10339–10343.CrossRefPubMedPubMedCentral
154.
Murata, T., Lin, M. I., Stan, R. V., Bauer, P. M., Yu, J., & Sessa, W. C. (2007). Genetic evidence supporting caveolae microdomain regulation of calcium entry in endothelial cells. Journal of Biological Chemistry, 282(22), 16631–16643.CrossRefPubMed
155.
Liao, Y., Plummer, N. W., George, M. D., Abramowitz, J., Zhu, M. X., & Birnbaumer, L. (2009). A role for Orai in TRPC-mediated Ca2 + entry suggests that a TRPC: Orai complex may mediate store and receptor operated Ca2+ entry. Proceedings of the National academy of Sciences of the United States of America, 106(9), 3202–3206.CrossRefPubMedPubMedCentral
156.
Lim, E. J., Majkova, Z., Xu, S., Bachas, L., Arzuaga, X., Smart, E., et al. (2008). Coplanar polychlorinated biphenyl-induced CYP1A1 is regulated through caveolae signaling in vascular endothelial cells. Chemico Biological Interactions, 176(2–3), 71–78.CrossRefPubMedPubMedCentral
Metadata
Title
Combustion Particle-Induced Changes in Calcium Homeostasis: A Contributing Factor to Vascular Disease?
Authors
Jørn A. Holme
Bendik C. Brinchmann
Eric Le Ferrec
Dominique Lagadic-Gossmann
Johan Øvrevik
Publication date
01-06-2019
Publisher
Springer US
Published in
Cardiovascular Toxicology / Issue 3/2019
Print ISSN: 1530-7905
Electronic ISSN: 1559-0259
DOI
https://doi.org/10.1007/s12012-019-09518-9

Other articles of this Issue 3/2019

Cardiovascular Toxicology 3/2019 Go to the issue

OriginalPaper

Late Cardiac Complications of Sulfur Mustard Poisoning in 38 Iranian Veterans

OriginalPaper

Cyclosporine Metabolites’ Metabolic Ratios May Be Markers of Cardiovascular Disease in Kidney Transplant Recipients Treated with Cyclosporine A-Based Immunosuppression Regimens

OriginalPaper

Vildagliptin, an Anti-diabetic Drug of the DPP-4 Inhibitor, Induces Vasodilation via Kv Channel and SERCA Pump Activation in Aortic Smooth Muscle

OriginalPaper

Digitalis Promotes Ventricular Arrhythmias in Flecainide- and Ranolazine-Pretreated Hearts

OriginalPaper

Cobalt Administration Causes Reduced Contractility with Parallel Increases in TRPC6 and TRPM7 Transporter Protein Expression in Adult Rat Hearts

OriginalPaper

Limb Blood Flow Restriction Plus Mild Aerobic Exercise Training Protects the Heart Against Isoproterenol-Induced Cardiac Injury in Old Rats: Role of GSK-3β

ACC 2024 Congress Coverage

Cardiology Video

Highlights from the ACC 2024 Congress

Watch now

Watch official videos from the ACC congress summarizing key highlights from the last year in heart failure, cardiomyopathies, valvular disease, pulmonary vascular disease, and pediatric cardiology.

Semaglutide benefits people with type 2 diabetes and obesity-related heart failure

16-04-2024 Type 2 Diabetes News

Incentivised to exercise

11-04-2024 Lifestyle Modifications News

New intervention for STEMI-related cardiogenic shock

10-04-2024 Myocardial Infarction News

» View more highlights on the ACC 2024 congress hub page

Image Credits