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It has been reported that exposure to infrasound causes cardiac dysfunction. Allowing for the key role of apoptosis in the pathogenesis of cardiovascular diseases, the objective of this study was to investigate the apoptotic effects of infrasound. Cardiac myocytes cultured from neonatal rats were exposed to infrasound of 5 Hz at 130 dB. The apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling. Also, the expression levels of a series of apoptosis-related proteins were detected. As a result, infrasound induced apoptosis of cultured rat cardiac myocytes in a time-dependant manner. The expression of proapoptotic proteins such as Bax, caspase-3, caspase-8, caspase-9, and FAS was significantly up-regulated, with concomitant down-regulated expression of antiapoptotic proteins such as Bcl-x, and the inhibitory apoptosis proteins family proteins including XIAP, cIAP-1, and cIAP-2. The expression of poly (ADP-ribose) polymerase and β-catenin, which are the substrate proteins of caspase-3, was significantly decreased. In conclusion, infrasound is an apoptotic inducer of cardiac myocytes. [ABSTRACT FROM AUTHOR]

1. Ageing has long been recognized as an independent risk factor for the development of cardiovascular diseases, contributing to high cardiovascular morbidity and mortality. Age-associated remodelling of the vascular wall includes luminal enlargement, intimal and medial thickening and vascular stiffness. 2. A growing body of evidence has indicated that the migration and proliferation of vascular smooth muscle cells (VSMC) play a pivotal role in the pathophysiological vascular ageing process. Both experimental and clinical evidence implicates platelet-derived growth factor (PDGF) as having an essential role in the proliferation of VSMC, an early pathological feature of arteriosclerosis and vascular ageing. 3. In the present review, we summarize some of the recent progress made with regard to defining the role of PDGF in the proliferation of VSMC and vascular ageing, with an emphasis on the cell signalling mechanisms involved. [ABSTRACT FROM AUTHOR]

To probe into the changes induced by infrasonic exposure on the methylation status of the genome in testes and underlying mechanisms, we inspected the percentage of unmethylated CpG sites (an index for DNA methylation level) and DNA methyltransferase activity in testes of SD rats exposed to infrasound of 8Hz at 90dB or 130dB for 1, 7, 14 and 21 days (2h/d). Compared to control groups at the same time points, significantly decreased DNA methylation level and methyltransferase activity were observed in all but experimental groups of id and 2 id at 90dB (p<0.05). Compared to 90dB groups at the same time points, DNA methylation level and DNA methyltransferase activity at 130dB decreased more significantly (p<0.05). The patterns of dynamic changes on the percentage of unmethylated CpG sites and methyltransferase activity at 130dB were different from those at 90dB. The results indicated that infrasonic exposure induced epigenetic changes in testes of rats, which depended on parameters of infrasonic exposure. [ABSTRACT FROM AUTHOR]