Similar articles

Abstract: Exposure to fine ambient particulate matter (PM_2.5) is known to be associated with cardiovascular disease. To uncover the molecular mechanisms involved in cardiovascular toxicity of PM_2.5, we investigated alterations in the protein profile of human umbilical vein endothelial cells (HUVECs) treated with PM_2.5 using two-dimensional electrophoresis in conjunction with mass spectrometry (MS). A total of 31 protein spots were selected as differentially expressed proteins and identified by matrix-assisted laser desorption/ionization-time of flight (MALDI-TOF) MS. The results demonstrated that DNA damage and cell apoptosis are important factors contributing to PM_2.5-mediated toxicity in HUVECs. It is further proposed that PM_2.5 can inhibit superoxide dismutase (SOD) activity and increase reactive oxygen species (ROS) and malonaldehyde (MDA) production in a concentration-dependent manner. Induction of apoptosis and DNA damage through oxidative stress pathways may be one of the key toxicological events occurring in HUVECs under PM_2.5 stress. These results indicated that the toxic mechanisms of PM_2.5 on cardiovascular disease are related to endothelial dysfunction.

大气细颗粒物PM_2.5对人脐静脉内皮细胞蛋白质组的影响

[1]Alaoui-Jamali MA, Xu YJ, 2006. Proteomic technology for biomarker profiling in cancer: an update. J Zhejiang Univ-Sci B, 7(6):411-420.

[2]Azad MB, Chen YQ, Gibson SB, 2009. Regulation of autophagy by reactive oxygen species (ROS):implications for cancer progression and treatment. Antioxid Redox Sign, 11(4):777-790.

[3]Brigelius-Flohe R, 2009. Commentary: oxidative stress reconsidered. Genes Nutr, 4(3):161-163.

[4]Brook RD, Rajagopalan S, Pope CA, 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.

[5]Burnett RT, Smith-Doiron M, Stieb D, et al., 1999. Effects of particulate and gaseous air pollution on cardiorespiratory hospitalizations. Arch Environ Health, 54(2):130-139.

[6]Calderón-Garcidueñas L, Villarreal-Calderon R, Valencia-Salazar G, et al., 2008. Systemic inflammation, endothelial dysfunction, and activation in clinically healthy children exposed to air pollutants. Inhal Toxicol, 20(5):499-506.

[7]Cheng Q, Yang CY, Guo BY, et al., 2017. Analysis of mechanism of PM2.5 and house dust mite antigen Der p1 in attack stage of child asthma. Eur Rev Med Pharmacol Sci, 21(10):2458-2462.

[8]Garneau D, Revil T, Fisette JF, et al., 2005. Heterogeneous nuclear ribonucleoprotein F/H proteins modulate the alternative splicing of the apoptotic mediator Bcl-x. J Biol Chem, 280(24):22641-22650.

[9]Ghio AJ, Carraway MS, Madden MC, 2012. Composition of air pollution particles and oxidative stress in cells, tissues, and living systems. J Toxicol Environ Health Part B, 15(1):1-21.

[10]Hirano S, Furuyama A, Koike E, et al., 2003. Oxidative-stress potency of organic extracts of diesel exhaust and urban fine particles in rat heart microvessel endothelial cells. Toxicology, 187(2-3):161-170.

[11]Lee BJ, Kim B, Lee K, 2014. Air pollution exposure and cardiovascular disease. Toxicol Res, 30(2):71-75.

[12]Lee IT, Yang CM, 2012. Role of NADPH oxidase/ROS in pro-inflammatory mediators-induced airway and pulmonary diseases. Biochem Pharmacol, 84(5):581-590.

[13]Li N, Hao MQ, Phalen RF, et al., 2003. Particulate air pollutants and asthma: a paradigm for the role of oxidative stress in PM-induced adverse health effects. Clin Immunol, 109(3):250-265.

[14]Li RJ, Kou XJ, Geng H, et al., 2014. Pollution characteristics of ambient PM_2.5-bound PAHs and NPAHs in a typical winter time period in Taiyuan. Chin Chem Lett, 25(5):663-666.

[15]Lu H, Daugherty A, 2013. Atherosclerosis: cell biology and lipoproteins. Curr Opin Lipidol, 24(1):107-108.

[16]Nicolas J, Chiari M, Crespo J, et al., 2008. Quantification of Saharan and local dust impact in an arid Mediterranean area by the positive matrix factorization (PMF) technique. Atmos Environ, 42(39):8872-8882.

[17]Pope CA, Burnctt RT, Thurston GD, et al., 2004. Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease. Circulation, 109(1):71-77.

[18]Rundell KW, Hoffman JR, Caviston R, et al., 2007. Inhalation of ultrafine and fine particulate matter disrupts systemic vascular function. Inhal Toxicol, 19(2):133-140.

[19]Singh R, Sharma BS, 2012. Composition, seasonal variation, and sources of PM₁₀ from world heritage site Taj Mahal, Agra. Environ Monit Assess, 184(10):5945-5956.

[20]Terzano C, Di Stefano F, Conti V, et al., 2010. Air pollution ultrafine particles: toxicity beyond the lung. Eur Rev Med Pharmacol Sci, 14(10):809-821.

[21]Torres-Ramos YD, Montoya-Estrada A, Guzman-Grenfell AM, et al., 2011. Urban PM2.5 induces ROS generation and RBC damage in COPD patients. Front Biosci, 3:808-817.

[22]Ucker DS, Jain MR, Pattabiraman G, et al., 2012. Externalized glycolytic enzymes are novel, conserved, and early biomarkers of apoptosis. J Biol Chem, 287(13):10325-10343.

[23]Vallejo M, Ruiz S, Hermosillo AG, et al., 2006. Ambient fine particles modify heart rate variability in young healthy adults. J Expo Sci Environ Epidemiol, 16(2):125-130.

[24]Wang JS, Tseng CY, Chao MW, 2017. Diesel exhaust particles contribute to endothelia apoptosis via autophagy pathway. Toxicol Sci, 156(1):72-83.

[25]Weichenthal SA, Godri-Pollitt K, Villeneuve PJ, 2013. PM_2.5, oxidant defence and cardiorespiratory health: a review. Environ Health, 12:40.

[26]Zhang HH, Li Z, Liu Y, et al., 2018. Physical and chemical characteristics of PM_2.5 and its toxicity to human bronchial cells BEAS-2B in the winter and summer. J Zhejiang Univ-Sci B (Biomed & Biotechnol), 19(4):317-326.