2125 In vivo molecular MRI of carotid artery injury in mice using an elastin-binding contrast agent
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Meeting abstract
2125 In vivo molecular MRI of carotid artery injury in mice using an elastin-binding contrast agent Marcus R Makowski*1, Ulrike Sausbier2, Yi Liu Liao2, Markus Schwaiger1, Winfried Neuhuber2, Simon Robinson3, Peter Ruth2, Matthias Sausbier2 and Rene M Botnar1 Address: 1Technische Universität München, Munich, Germany, 2Institut für Pharmazie, Tübingen, Germany and 3Bristol-Myers Squibb Medical Imaging, North Billerica, MA, USA * Corresponding author
from 11th Annual SCMR Scientific Sessions Los Angeles, CA, USA. 1–3 February 2008 Published: 22 October 2008 Journal of Cardiovascular Magnetic Resonance 2008, 10(Suppl 1):A394
doi:10.1186/1532-429X-10-S1-A394
Abstracts of the 11th Annual SCMR Scientific Sessions - 2008
Meeting abstracts – A single PDF containing all abstracts in this Supplement is available here. http://www.biomedcentral.com/content/pdf/1532-429X-10-S1-info.pdfThis abstract is available from: http://jcmr-online.com/content/10/S1/A394 © 2008 Makowski et al; licensee BioMed Central Ltd.
Introduction Smooth muscle cell proliferation and extracellular matrix (ECM) synthesis/turnover are thought to play an important role in vessel wall repair after vascular injury. Recently, we identified the cysteine-rich-protein-2 (CRP2) as novel and specific molecular effector of the NO/cGMP/ cGMP-dependent-protein-kinase-I (PKG) signaling in vascular smooth muscle. To elucidate whether CRP2 contributes to the postulated pro-proliferative/proatherogenic effect of PKG, we established a CRP2-deficient mouse line by targeted deletion of the exons 2–7 in the CRP2-gene. With the simultaneous development of a novel ECM-specific MR contrast agent (BMS753951) non-invasive assessment of changes in remodeling of the injured mouse carotid wall has become feasible.
Purpose In this study we investigated whether the use of an elastinbinding contrast agent would allow the detection of vascular remodeling in a mouse model of carotid artery injury and whether it would facilitate the detection of impaired ECM formation in CRP2-/- mice.
Methods A carotid artery injury model was performed in 8 wildtype and 8 CRP2-deficient (CRP2-/-) mice; the right carotid artery wall was damaged, while the left served as control. Two month after surgical intervention, MRI of the
carotid vessel walls was performed in a 1.5 T Philips Achieva clinical MR scanner using a single loop small animal coil, a dedicated cardiac software package (R1.2.2) and a clinical gradient system (30 mT/m, 150 mT/m/ms). Time-of-flight angiography of the carotid arteries was performed for visualization of the injured vessel segment and for subsequent planning of the vessel wall scans. Imaging parameters included TR = 43, TE = 8.1, flip angel = 60°, spatial resolution = 0.2 × 0.2 × 0.5 mm. For assessment of ECM remodeling, an inversion recovery vessel wall sequence was performed approximately 45–60 minutes post injection of 0.1 mmol/kg of BMS753951 (BristolMyer-Squibb/Billerica/MA), a novel elastin-binding Gdbased cont
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