Ambient air particulate matter exposure and tissue factor expression in atherosclerosis

Qinghua Sun, Peibin Yue, Rita I. Kirk, Aixia Wang, Didier Moatti, Ximei Jin, Bo Lu, Alison D. Schecter, Morton Lippmann, Terry Gordon, Lung Chi Chen, Sanjay Rajagopalan

Research output: Contribution to journalArticlepeer-review

98 Scopus citations

Abstract

Recent studies have suggested a link between inhaled particulate matter (PM) exposure and atherogenesis. We investigated tissue factor (TF) expression with ambient fine particulate matter (diameter < 2.5 μm, PM2.5) exposure and in response to in vitro exposure to fine and ultrafine PM in cultured human bronchial epithelial cells, vascular smooth muscle cells (hSMCs), and monocytes. ApoE-/- mice, fed with normal chow (NC) or high-fat chow (HFC), were exposed to concentrated PM2.5 or filtered air (FA) for 6 mo (6 h/day, 5 day/wk, n = 28). Following in vivo ultrasound bio-microscopy (UBM) assessment of plaque area, macrophage infiltration (CD68) and TF expression in the aorta were quantified. Cultured cells were incubated with size-fractionated PM from cascade impactors, or with standard reference PM material (SRM, number 1649a) and assayed for TF protein, mRNA, and activity. UBM-derived plaque areas were 7 ± 1% larger in the PM2.5-HFC than the FA-HFC group (p =.04), but not significantly different between the PM2.5-NC and FA-NC groups (p =.07). Immunohistochemistry revealed increased TF (15 ± 3% vs. 8 ± 2%, p <.01) and macrophage infiltration (19 ± 2% vs. 14 ± 3%, p <.01) in the plaques of PM2.5-HFC compared with FA-HFC groups. Impactor-collected PM2.5 and ultrafine particles consistently increased TF protein in bronchial epithelial cells, monocytes, and hSMCs. TF mRNA expression increased rapidly (within 1 h) in response to SRM PM. We conclude that in vivo and in vitro exposure to ambient air PM2.5 induces TF expression.

Original languageEnglish
Pages (from-to)127-137
Number of pages11
JournalInhalation Toxicology
Volume20
Issue number2
DOIs
StatePublished - Jan 2008

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