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The anti-microbial peptide SR-0379 stimulates human endothelial progenitor cell-mediated repair of peripheral artery diseases

  • Lee, Tae Wook (Department of Physiology, School of Medicine, Pusan National University) ;
  • Heo, Soon Chul (Department of Physiology, School of Medicine, Pusan National University) ;
  • Kwon, Yang Woo (Department of Physiology, School of Medicine, Pusan National University) ;
  • Park, Gyu Tae (Department of Physiology, School of Medicine, Pusan National University) ;
  • Yoon, Jung Won (Department of Physiology, School of Medicine, Pusan National University) ;
  • Kim, Seung-Chul (Department of Obstetrics and Gynecology, School of Medicine, Pusan National University) ;
  • Jang, Il Ho (Department of Oral Biochemistry and Molecular Biology, Pusan National University School of Dentistry) ;
  • Kim, Jae Ho (Department of Physiology, School of Medicine, Pusan National University)
  • Received : 2017.03.10
  • Accepted : 2017.05.23
  • Published : 2017.10.31

Abstract

Ischemia is a serious disease, characterized by an inadequate blood supply to an organ or part of the body. In the present study, we evaluated the effects of the anti-microbial peptide SR-0379 on the stem cell-mediated therapy of ischemic diseases. The migratory and tube-forming abilities of human endothelial progenitor cells (EPCs) were enhanced by treatment with SR-0379 in vitro. Intramuscular administration of SR-0379 into a murine ischemic hindlimb significantly enhanced blood perfusion, decreased tissue necrosis, and increased the number of blood vessels in the ischemic muscle. Moreover, co-administration of SR-0379 with EPCs stimulated blood perfusion in an ischemic hindlimb more than intramuscular injection with either SR-0379 or EPCs alone. This enhanced blood perfusion was accompanied by a significant increase in the number of CD31- and ${\alpha}$-SMA-positive blood vessels in ischemic hindlimb. These results suggest that SR-0379 is a potential drug candidate for potentiating EPC-mediated therapy of ischemic diseases.

Keywords

References

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