Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 118, Issue 44, Pages -Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.2108131118
Keywords
silica nanoparticle; corona; apolipoprotein A-I; cardiovascular damage; atherosclerosis
Categories
Funding
- National Natural Sci-ence Foundation of China [21976145, 22176206]
- Fundamental Research Funds for the Central Universities [XDJK2019TJ001]
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This study found that upon respiratory exposure to silica nanoparticles (SiNPs), mice exhibited on-site cardiovascular damage. SiNPs adsorbed apolipoprotein A-I (Apo A-I) to mitigate toxic effects, but eventually depleted Apo A-I leading to unexpected toxic effects. The findings suggest a potential mechanism for the cardiovascular effects of nanoparticles.
The rapid development of nanotechnology has greatly benefited modern science and engineering and also led to an increased environmental exposure to nanoparticles (NPs). While recent research has established a correlation between the exposure of NPs and cardiovascular diseases, the intrinsic mechanisms of such a connection remain unclear. Inhaled NPs can penetrate the air-blood barrier from the lung to systemic circulation, thereby intruding the cardiovascular system and generating cardiotoxic effects. In this study, on-site cardiovascular damage was observed in mice upon respiratory exposure of silica nanoparticles (SiNPs), and the corresponding mechanism was investigated by focusing on the interaction of SiNPs and their encountered biomacromolecules en route. SiNPs were found to collect a significant amount of apolipoprotein A-I (Apo A-I) from the blood, in particular when the SiNPs were preadsorbed with pulmonary surfactants. While the adsorbed Apo A-I ameliorated the cytotoxic and proinflammatory effects of SiNPs, the protein was eliminated from the blood upon clearance of the NPs. However, supplementation of Apo A-I mimic peptide mitigated the atherosclerotic lesion induced by SiNPs. In addition, we found a further declined plasma Apo A-I level in clinical silicosis patients than coronary heart disease patients, suggesting clearance of SiNPs sequestered Apo A-I to compromise the corona! protein's regular biological functions. Together, this study has provided evidence that the protein corona of SiNPs acquired in the blood depletes Apo A-I, a biomarker for prediction of cardiovascular diseases, which gives rise to unexpected toxic effects of the nanoparticles.
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