TY - JOUR
T1 - Ambient air particulate matter exposure and tissue factor expression in atherosclerosis
AU - Sun, Qinghua
AU - Yue, Peibin
AU - Kirk, Rita I.
AU - Wang, Aixia
AU - Moatti, Didier
AU - Jin, Ximei
AU - Lu, Bo
AU - Schecter, Alison D.
AU - Lippmann, Morton
AU - Gordon, Terry
AU - Chen, Lung Chi
AU - Rajagopalan, Sanjay
N1 - Funding Information:
Received 10 July 2007; accepted 28 September 2007. This work was supported by grants from the NIH (RO1 ES013406 and ES015146) to Dr. Rajagopalan and by U.S. EPA and NIEHS grants (R827351, ES00260) to Dr. Lippmann. Address correspondence to Sanjay Rajagopalan, MD, Davis Heart & Lung Research Institute, 473 W. 12th Avenue, Room 110, Columbus, OH 43210, USA. E-mail: [email protected]; or Lung Chi Chen, PhD, Department of Environmental Medicine, New York University School of Medicine, 57 Old Forge Road, Tuxedo, NY 10987, USA. E-mail: [email protected]
PY - 2008/1
Y1 - 2008/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=38849153451&partnerID=8YFLogxK
U2 - 10.1080/08958370701821482
DO - 10.1080/08958370701821482
M3 - Article
C2 - 18236227
AN - SCOPUS:38849153451
SN - 0895-8378
VL - 20
SP - 127
EP - 137
JO - Inhalation Toxicology
JF - Inhalation Toxicology
IS - 2
ER -