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 Blood, 1 January 2009, Vol. 113, No. 1, pp. 233-243.
Prepublished online as a Blood First Edition Paper on October 2, 2008; DOI 10.1182/blood-2008-06-162891.

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Submitted June 13, 2008
Accepted August 30, 2008

Endothelial progenitor cell homing: prominent role of the IGF2-IGF2R-PLC{beta}2 axis

Yong-Sun Maeng, Hyun-Jung Choi, Ja-Young Kwon, Yong-Won Park, Kyu-Sil Choi, Jeong-Ki Min, Yun-Hee Kim, Pann-Ghill Suh, Kyung-Sun Kang, Moo-Ho Won, Young-Myeong Kim, and Young-Guen Kwon*

Department of Biochemistry, College of Life Sciences and Biotechnology, Yonsei University, Seoul, Korea, Republic of
Department of Obstetrics and Gynecology, Yonsei University College of Medicine, Seoul, Korea, Republic of
Department of Radiology, Insitute for Radiological Imaging Science, Wonkwang University School of Medicine, Iksan, Korea, Republic of
Therapeutic Antibody Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea, Republic of
Department of Life Science, Division of Molecular and Life Science, Pohang University of Science and Technology, Pohang, Korea, Republic of
Laboratory of Stem Cell and Tumor Biology, College of Veterinary Medicine, Seoul National University, Seoul, Korea, Republic of
Department of Anatomy, College of Medicine, Hallym University, Chuncheon, Korea, Republic of
Department of Molecular and Cellular Biochemistry, School of Medicine, Kangwon National University, Chuncheon, Korea, Republic of

* Corresponding author; email: ygkwon{at}yonsei.ac.kr.

Homing of endothelial progenitor cells (EPCs) to the neovascular zone is now considered to be an essential step in the formation of vascular networks during embryonic development and also for neovascularization in postnatal life. We report here the prominent role of the insulin-like growth factor 2 (IGF2)/IGF2 receptor (IGF2R) system in promoting EPC homing. With high-level expression of IGF2R in EPCs, IGF2-induced hypoxic conditions stimulated multiple steps of EPC homing in vitro and promoted both EPC recruitment and incorporation into the neovascular area, resulting in enhanced angiogenesis in vivo. Remarkably, all IGF2 actions were exerted predominantly through IGF2R-linked G(i) protein signaling and required intracellular Ca2+ mobilization induced by the {beta}2 isoform of phospholipase C. Together, these findings indicate that locally generated IGF2 at either ischemic or tumor sites may contribute to postnatal vasculogenesis by augmenting the recruitment of EPCs. The utilization of the IGF2/IGF2R system may therefore be useful for the development of novel means to treat angiogenesis-dependent diseases.


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