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. 2008 Jun;28(6):1117-22.
doi: 10.1161/ATVBAHA.108.165589. Epub 2008 Apr 10.

Ultrasonic Microbubble Destruction Stimulates Therapeutic Arteriogenesis via the CD18-dependent Recruitment of Bone Marrow-Derived Cells

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Ultrasonic Microbubble Destruction Stimulates Therapeutic Arteriogenesis via the CD18-dependent Recruitment of Bone Marrow-Derived Cells

John C Chappell et al. Arterioscler Thromb Vasc Biol. .

Abstract

Objective: We have previously shown that, under certain conditions, ultrasonic microbubble destruction creates arteriogenesis and angiogenesis in skeletal muscle. Here, we tested whether this neovascularization response enhances hyperemia in a rat model of arterial insufficiency and is dependent on the recruitment of bone marrow-derived cells (BMDCs) to treated tissues via a beta2 integrin (CD18)-dependent mechanism.

Methods and results: Sprague-Dawley rats, C57BL/6 wild-type mice, and C57BL/6 chimeric mice engrafted with BMDCs from either GFP+ or CD18-/- mice received bilateral femoral artery ligations. Microbubbles (MBs) were intravenously injected, and one gracilis muscle was exposed to pulsed 1 MHz ultrasound (US). Rat hindlimbs exhibited significant increases in adenosine-induced hyperemia and arteriogenesis compared to contralateral controls at 14 and 28 days posttreatment. US-MB-treated wild-type C57BL/6 mice exhibited significant arteriogenesis, angiogenesis, and CD11b+ monocyte recruitment; however, these responses were all completely blocked in CD18-/- chimeric mice. The number of BMDCs increased in US-MB-treated muscles of GFP+ chimeric mice; however, GFP+ BMDCs did not incorporate into microvessels as vascular cells.

Conclusions: In skeletal muscle affected by arterial occlusion, arteriogenesis and hyperemia can be significantly enhanced by ultrasonic MB destruction. This response depends on the recruitment, but not vascular incorporation, of BMDCs via a CD18-dependent mechanism.

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