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Anthropogenic noise of variable temporal patterns is increasing in aquatic environments, causing physiological stress and sensory impairment. However, scarce information exists on exposure effects to continuous versus intermittent disturbances, which is critical for noise sustainable management. We tested the effects of different noise regimes on the auditory system and behaviour in the zebrafish (Danio rerio). Adult zebrafish were exposed for 24 h to either white noise (150 ± 10 dB re 1 μPa) or silent control. Acoustic playbacks varied in temporal patterns—continuous, fast and slow regular intermittent, and irregular intermittent. Auditory sensitivity was assessed with Auditory Evoked Potential recordings, revealing hearing loss and increased response latency in all noise-treated groups. The highest mean threshold shifts (c. 13 dB) were registered in continuous and fast intermittent treatments, and no differences were found between regular and irregular regimes. Inner ear saccule did not reveal significant hair cell loss but showed a decrease in presynaptic Ribeye b protein especially after continuous exposure. Behavioural assessment using the standardized Novel Tank Diving assay showed that all noise-treated fish spent > 98% time in the bottom within the first minute compared to 82% in control, indicating noise-induced anxiety/stress. We provide first data on how different noise time regimes impact a reference fish model, suggesting that overall acoustic energy is more important than regularity when predicting noise effects.
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Anthropogenic noise can be hazardous for the auditory system and wellbeing of animals, including humans. However, very limited information is known on how this global environmental pollutant affects auditory function and inner ear sensory receptors in early ontogeny. The zebrafish (Danio rerio) is a valuable model in hearing research, including investigations of developmental processes of the vertebrate inner ear. We tested the effects of chronic exposure to white noise in larval zebrafish on inner ear saccular sensitivity and morphology at 3 and 5 days post-fertilization (dpf), as well as on auditory-evoked swimming responses using the prepulse inhibition (PPI) paradigm at 5 dpf. Noise-exposed larvae showed a significant increase in microphonic potential thresholds at low frequencies, 100 and 200 Hz, while the PPI revealed a hypersensitization effect and a similar threshold shift at 200 Hz. Auditory sensitivity changes were accompanied by a decrease in saccular hair cell number and epithelium area. In aggregate, the results reveal noise-induced effects on inner ear structure–function in a larval fish paralleled by a decrease in auditory-evoked sensorimotor responses. More broadly, this study highlights the importance of investigating the impact of environmental noise on early development of sensory and behavioural responsiveness to acoustic stimuli.
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AimsVascular calcification is a common clinical complication of chronic kidney disease (CKD), atherosclerosis (AS), and diabetes, which is associated with increased cardiovascular morbidity and mortality in patients. The transdifferentiation of vascular smooth muscle cells (VSMCs) to an osteochondrogenic phenotype is a crucial step during vascular calcification. The transcription factor CCAAT/enhancer-binding protein alpha (C/EBPα) plays an important role in regulating cell proliferation and differentiation, but whether it regulates the calcification of arteries and VSMCs remains unclear. Therefore, this study aims to understand the role of C/EBPα in the regulation of vascular calcification.Methods and ResultsBoth mRNA and protein expression levels of C/EBPα were significantly increased in calcified arteries from mice treated with a high dose of vitamin D3 (vD3). Upregulation of C/EBPα was also observed in the high phosphate- and calcium-induced VSMC calcification process. The siRNA-mediated knockdown of C/EBPα significantly attenuated VSMC calcification in vitro. Moreover, C/EBPα depletion in VSMCs significantly reduced the mRNA expression of the osteochondrogenic genes, e.g., sex-determining region Y-box 9 (Sox9). C/EBPα overexpression can induce SOX9 overexpression. Similar changes in the protein expression of SOX9 were also observed in VSMCs after C/EBPα depletion or overexpression. In addition, silencing of Sox9 expression significantly inhibited the phosphate- and calcium-induced VSMC calcification in vitro.ConclusionFindings in this study indicate that C/EBPα is a key regulator of the osteochondrogenic transdifferentiation of VSMCs and vascular calcification, which may represent a novel therapeutic target for vascular calcification.