Ambient air particulate matter exposure and tissue factor expression in atherosclerosis
Autor: | Peibin Yue, Didier Moatti, Sanjay Rajagopalan, Ximei Jin, Qinghua Sun, Bo Lu, Morton Lippmann, Rita I Kirk, Aixia Wang, Lung Chi Chen, Alison D. Schecter, Terry Gordon |
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Rok vydání: | 2008 |
Předmět: |
Male
Pathology medicine.medical_specialty Vascular smooth muscle Health Toxicology and Mutagenesis Bronchi Toxicology Monocytes Muscle Smooth Vascular Thromboplastin Tissue factor Mice Apolipoproteins E In vivo Air Pollution Ultrafine particle medicine Image Processing Computer-Assisted Animals Humans Gene Silencing RNA Messenger Cells Cultured Ultrasonography Inhalation exposure Mice Knockout Inhalation Exposure Dose-Response Relationship Drug Chemistry CD68 Epithelial Cells Environmental Exposure Atherosclerosis Molecular biology Dose–response relationship Disease Models Animal Gene Expression Regulation Immunohistochemistry Particulate Matter |
Zdroj: | Inhalation toxicology. 20(2) |
ISSN: | 1091-7691 |
Popis: | 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 microm, PM(2.5)) 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 PM(2.5) 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 PM(2.5)-HFC than the FA-HFC group (p = .04), but not significantly different between the PM(2.5)-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 PM(2.5)-HFC compared with FA-HFC groups. Impactor-collected PM(2.5) 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 PM(2.5) induces TF expression. |
Databáze: | OpenAIRE |
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