| First Author | Li R | Year | 2013 |
| Journal | Am J Physiol Cell Physiol | Volume | 304 |
| Issue | 4 | Pages | C362-9 |
| PubMed ID | 23242187 | Mgi Jnum | J:194848 |
| Mgi Id | MGI:5474905 | Doi | 10.1152/ajpcell.00322.2012 |
| Citation | Li R, et al. (2013) Atmospheric ultrafine particles promote vascular calcification via the NF-kappaB signaling pathway. Am J Physiol Cell Physiol 304(4):C362-9 |
| abstractText | Exposure to atmospheric fine particulate matter (PM(2.5)) is a modifiable risk factor of cardiovascular disease. Ultrafine particles (UFP, diameter <0.1 mum), a subfraction of PM(2.5), promote vascular oxidative stress and inflammatory responses. Epidemiologic studies suggest that PM exposure promotes vascular calcification. Here, we assessed whether UFP exposure promotes vascular calcification via NF-kappaB signaling. UFP exposure at 50 mug/ml increased alkaline phosphatase (ALP) activity by 4.4 +/- 0.2-fold on day 3 (n = 3, P < 0.001) and matrix calcification by 3.5 +/- 1.7-fold on day 10 (n = 4, P < 0.05) in calcifying vascular cells (CVC), a subpopulation of vascular smooth muscle cells with osteoblastic potential. Treatment of CVC with conditioned media derived from UFP-treated macrophages (UFP-CM) also led to an increase in ALP activities and matrix calcification. Furthermore, both UFP and UFP-CM significantly increased NF-kappaB activity, and cotreatment with an NF-kappaB inhibitor, JSH23, attenuated both UFP- and UFP-CM-induced ALP activity and calcification. When low-density lipoprotein receptor-null mice were exposed to UFP at 359.5 mug/m(3) for 10 wk, NF-kappaB activation and vascular calcification were detected in the regions of aortic roots compared with control filtered air-exposed mice. These findings suggest that UFP promotes vascular calcification via activating NF-kappaB signaling. |
