Erschienen in:
Open Access
01.06.2013 | Poster presentation
Bone morphogenetic protein-2 and leptin but not endothelin-1 induce osteochondrogenesis through increasing oxidative stress in vascular smooth muscle cells
verfasst von:
LS do Carmo, MCC de Andrade, D de Castro Fernandes, M Liberman
Erschienen in:
Critical Care
|
Sonderheft 3/2013
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Excerpt
Vascular calcification is a regulated process, which associates with coronary artery disease (CAD) and occurs through an increase in transcription factor expression such as RUNX2, MSX2 and alkaline phosphatase (ALP), then inducing calcium deposition. Bone morphogenetic protein-2 (BMP2) is a potent osteochondrogenic mediator, which is expressed in CAD. Endothelin-1 (ET1) and leptin have a role in regulating inflammation and CAD. We hypothesized that BMP2, leptin or both increase ROS formation in C57BL/6 vascular smooth muscle cells (SMC), stimulating osteochondrogenic differentiation. We also investigated the effect of ET1 in SMC osteochondrogenesis. Our objectives were: to investigate ROS production in SMC after BMP2 (50 ng/ml) and/or leptin (10 ng/ml) incubation for 6 hours; and to assess osteochondrogenic gene expression and calcification of SMC stimulated with BMP2, leptin or ET1 (10 nM). …