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 alterat...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.展开更多
基金Supported by National Natural Science Foundation of China No.81000169,No.81100277,No.81370008,and No.81200284the Excellent Young Investigator Foundation of the Health Bureau of Zhejiang Province No.2010QNA011+2 种基金the Excellent Young Investigator Natural Science Foundation of Zhejiang Province No.R2110159the Project of Zhejiang Traditional Chinese Medicine Administration Bureau No.2010ZA065the Fundamental Research Funds for the Central Universities No.2013QNA702
文摘AIM: To explore mitochondrial dysfunction in nonalcoholic steatohepatitis (NASH) by analyzing the proteome of liver mitochondria from a NASH model.
基金Project supported by the Medical and Health Science and Technology Fund of Zhejiang Province(No.2016KYB224)the Scientific Research Fund of Zhejiang Chinese Medicine University(No.2015ZG17),China
文摘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.
