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Molecular Imaging of Activated Matrix Metalloproteinases in Vascular Remodeling

Identifieur interne : 006247 ( Main/Repository ); précédent : 006246; suivant : 006248

Molecular Imaging of Activated Matrix Metalloproteinases in Vascular Remodeling

Auteurs : RBID : Pascal:08-0527236

Descripteurs français

Pascal (Inist)
- Pathologie de l'appareil circulatoire, Remodelage vasculaire, Imagerie moléculaire.

English descriptors

KwdEn :
- Cardiovascular disease, Molecular imaging, Vascular remodeling.

Abstract

Background-Matrix metalloproteinase (MMP) activation plays a key role in vascular remodeling. RP782 is a novel indium ¹¹¹In-labeled tracer with specificity for activated MMPs. We hypothesized that RP782 can detect injury-induced vascular remodeling in vivo. Methods and Results-Left common carotid artery injury was induced with a guidewire in apolipoprotein E^-/- mice. Sham surgery was performed on the contralateral artery, which served as control for imaging experiments. Carotid wire injury led to significant hyperplasia and expansive remodeling over a period of 4 weeks. MMP activity, detected by in situ zymography, increased in response to injury and was maximal by 3 to 4 weeks after injury. RP782 (11.1 MBq) was injected intravenously into apolipoprotein E^-/- mice at 1, 2, 3, and 4 weeks after left carotid injury. MicroSPECT imaging was performed at 2 hours and was followed by CT angiography to localize the carotid arteries. In vivo images revealed focal uptake of RP782 in the injured carotid artery at 2, 3, and 4 weeks. Increased tracer uptake in the injured artery was confirmed by quantitative autoradiography. Pretreatment with 50-fold excess nonlabeled tracer significantly reduced RP782 uptake in injured carotids, thus demonstrating uptake specificity. Weekly changes in the vessel-wall area closely paralleled and correlated with RP782 uptake (Spearman r=0.95, P=0.001). Conclusions-Injury-induced MMP activation in the vessel wall can be detected by RP782 microSPECT/CT imaging in vivo. RP782 uptake tracks the hyperplastic process in vascular remodeling and provides an opportunity to track the remodeling process in vivo.

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<author><name sortKey="Azure, Michael" uniqKey="Azure M">Michael Azure</name>
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<author><name sortKey="Sinusas, Albert J" uniqKey="Sinusas A">Albert J. Sinusas</name>
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<author><name sortKey="Sadeghi, Mehran M" uniqKey="Sadeghi M">Mehran M. Sadeghi</name>
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<title level="j" type="abbreviated">Circulation : (N. Y. N.Y.)</title>
<title level="j" type="main">Circulation : (New York, N.Y.)</title>
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<front><div type="abstract" xml:lang="en">Background-Matrix metalloproteinase (MMP) activation plays a key role in vascular remodeling. RP782 is a novel indium <sup>111</sup>
In-labeled tracer with specificity for activated MMPs. We hypothesized that RP782 can detect injury-induced vascular remodeling in vivo. Methods and Results-Left common carotid artery injury was induced with a guidewire in apolipoprotein E<sup>-/-</sup>
 mice. Sham surgery was performed on the contralateral artery, which served as control for imaging experiments. Carotid wire injury led to significant hyperplasia and expansive remodeling over a period of 4 weeks. MMP activity, detected by in situ zymography, increased in response to injury and was maximal by 3 to 4 weeks after injury. RP782 (11.1 MBq) was injected intravenously into apolipoprotein E<sup>-/-</sup>
 mice at 1, 2, 3, and 4 weeks after left carotid injury. MicroSPECT imaging was performed at 2 hours and was followed by CT angiography to localize the carotid arteries. In vivo images revealed focal uptake of RP782 in the injured carotid artery at 2, 3, and 4 weeks. Increased tracer uptake in the injured artery was confirmed by quantitative autoradiography. Pretreatment with 50-fold excess nonlabeled tracer significantly reduced RP782 uptake in injured carotids, thus demonstrating uptake specificity. Weekly changes in the vessel-wall area closely paralleled and correlated with RP782 uptake (Spearman r=0.95, P=0.001). Conclusions-Injury-induced MMP activation in the vessel wall can be detected by RP782 microSPECT/CT imaging in vivo. RP782 uptake tracks the hyperplastic process in vascular remodeling and provides an opportunity to track the remodeling process in vivo.</div>
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 mice. Sham surgery was performed on the contralateral artery, which served as control for imaging experiments. Carotid wire injury led to significant hyperplasia and expansive remodeling over a period of 4 weeks. MMP activity, detected by in situ zymography, increased in response to injury and was maximal by 3 to 4 weeks after injury. RP782 (11.1 MBq) was injected intravenously into apolipoprotein E<sup>-/-</sup>
 mice at 1, 2, 3, and 4 weeks after left carotid injury. MicroSPECT imaging was performed at 2 hours and was followed by CT angiography to localize the carotid arteries. In vivo images revealed focal uptake of RP782 in the injured carotid artery at 2, 3, and 4 weeks. Increased tracer uptake in the injured artery was confirmed by quantitative autoradiography. Pretreatment with 50-fold excess nonlabeled tracer significantly reduced RP782 uptake in injured carotids, thus demonstrating uptake specificity. Weekly changes in the vessel-wall area closely paralleled and correlated with RP782 uptake (Spearman r=0.95, P=0.001). Conclusions-Injury-induced MMP activation in the vessel wall can be detected by RP782 microSPECT/CT imaging in vivo. RP782 uptake tracks the hyperplastic process in vascular remodeling and provides an opportunity to track the remodeling process in vivo.</s0>
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Molecular Imaging of Activated Matrix Metalloproteinases in Vascular Remodeling

Molecular Imaging of Activated Matrix Metalloproteinases in Vascular Remodeling

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