Effects of polystyrene nanoplastics on endothelium senescence and its underlying mechanism

Global plastic use has increased rapidly, and environmental pollution associated with nanoplastics (NPs) has been a growing concern recently. However, the impact and biological mechanism of NPs on the cardiovascular system are not well characterized. This study aimed to assess the possibility that N...

Full description

Saved in:

Bibliographic Details
Published in:	Environment international Vol. 164; p. 107248
Main Authors:	Shiwakoti, Saugat, Ko, Ju-Young, Gong, Dalseong, Dhakal, Bikalpa, Lee, Jeong-Hye, Adhikari, Radhika, Gwak, Yeonhyang, Park, Sin-Hee, Jun Choi, Ik, Schini-Kerth, Valérie B., Kang, Ki-Woon, Oak, Min-Ho
Format:	Journal Article
Language:	English
Published:	Netherlands Elsevier Ltd 01-06-2022 Elsevier
Subjects:	Endothelial cell senescence NADPH oxidase Nanoplastics Oxidative stress Sirt1 Oxidative stress Endothelial cell senescence Sirt1 NADPH oxidase Nanoplastics
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	Global plastic use has increased rapidly, and environmental pollution associated with nanoplastics (NPs) has been a growing concern recently. However, the impact and biological mechanism of NPs on the cardiovascular system are not well characterized. This study aimed to assess the possibility that NPs exposure promotes premature endothelial cell (EC) senescence in porcine coronary artery ECs and, if so, to elucidate the underlying mechanism. Treatment of ECs with NPs promoted the acquisition of senescence markers, senescence-associated β-galactosidase activity, and p53, p21, and p16 protein expression, resulting in the inhibition of proliferation. In addition, NPs impaired endothelium-dependent vasorelaxation associated with decreased endothelial nitric oxide synthase (eNOS) expression. NPs enhanced reactive oxygen species formation in ECs, and increased oxidative stress levels were associated with the induction of NADPH oxidases expression, followed by the subsequent downregulation of Sirt1 expression. The characteristics of EC senescence and dysfunction caused by NPs are prevented by an antioxidant (N-acetylcysteine), an NADPH oxidase inhibitor (apocynin), and a Sirt1 activator (resveratrol). These findings indicate that NPs induced premature EC senescence, at least in part, through the redox-sensitive eNOS/Sirt1 signaling pathway. This study suggested the effects and underlying mechanism of NPs on the cardiovascular system, which may provide pharmacological targets to prevent NPs-associated cardiovascular diseases.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0160-4120 1873-6750
DOI:	10.1016/j.envint.2022.107248