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1 Life Science and Bioethics Research Center, Tokyo Med Dent Univ, Tokyo, NA, Japan
2 Tokyo, NA, Japan; Life Science and Bioethics Research Center, Tokyo Med Dent Univ, Tokyo, NA, Japan
3 Biochemistry, Keio University, Tokyo, Japan
4 Biochemistry, Keio University, United States
* To whom correspondence should be addressed. E-mail: masavasc{at}tmd.ac.jp.
Wire injury of an artery has been recognized as a standard model of vascular inflammation and atherosclerosis; however, the mechanism of leukocyte recruitment has not been studied in this model. In this study, we documented the recruitment of leukocytes to the murine femoral artery after a wire injury. A transluminal mechanical injury was generated by inserting a wire to the femoral artery of male C57BL/6J mice. Mice, anesthetized and ventilated after tracheotomy, were protected from hypothermia by a warming lamp. Body temperatures and blood pH did not significantly change during the experiment. The interaction between Rhodamine-6G labeled leukocytes and the injured femoral artery was monitored using an epifluorescent microscope. The captured images were then evaluated using a computer-assisted image analysis program. In the absence of injury, virtually no leukocyte adhesion was observed. In contrast, the number of adherent leukocytes increased at 4 hours and at 24 hours after injury. The number of leukocyte adhesion was reduced when we examined those 72 hours after injury. The rolling flux of leukocytes increased at 4 hours and remained high up to 7 days, whereas its velocity was faster at 72 hours. Further, we identified another peak of leukocyte adhesion at 7 days after injury. Injection of anti-P-selectin antibody significantly reduced leukocyte adhesion at the early and the later phase. In conclusion, we have established a novel experimental system to directly observe leukocyte recruitment to the injured femoral artery. Our system revealed a previously undetected, unique profile of leukocyte recruitment during vascular injury.
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