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Therapeutic arteriogenesis by ultrasonic microbubble destruction requires the recruitment of bone‐marrow derived cells through a CD18 dependent pathway
Author(s) -
Chappell John Christopher,
Huang Judith,
Price Richard
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1217
Subject(s) - arteriogenesis , bone marrow , medicine , cd18 , femoral artery , sma* , hindlimb , anatomy , pathology , ischemia , integrin , receptor , mathematics , combinatorics
We have shown that ultrasonic microbubble (MB) destruction induces arteriogenesis in normal mouse gracilis muscle (GM) ( Ultr Med Biol . 2005(31)1411). Here, we tested the hypothesis that MB interactions with ultrasound (US) induce arteriogenesis in ischemic GM via CD18 dependent recruitment of bone marrow cells (BMCs). BMCs from CD18 −/− mice were transplanted into irradiated wild‐type (WT) mice and allowed to reconstitute for 8 weeks. WT and CD18 chimeric mice were given bilateral femoral artery ligations. After 3 days, mice received US+MB treatment in one GM and sham treatment in the contralateral GM. After 3 more days, GMs were fluorescently‐labeled for smooth muscle α‐actin (SMA) and analyzed for arteriogenesis. In WT mice, there was no difference in arterial trees and loops between treatment groups. The length density of SMA+ vessels in US+MB treated GMs of WT mice was significantly greater than sham GMs. As compared to sham, WT treated muscles also exhibited a significant 45% increase in intersections between SMA+ vessels and seven equally spaced lines perpendicular to fiber direction (US+MB: 128+/−8 vs SHAM: 89+/−8). In contrast, US+MB‐treated GMs in CD18 chimeras showed no difference in these intersections (US+MB: 93+/−7 vs. SHAM: 93+/−12). We conclude that ultrasonic MB destruction elicits arteriogenesis via recruitment of BMCs to treated muscle through CD18. Supported by AHA0555511U and NIH HL74082.

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