The chemokine receptor CXCR4 is essential for vascularization of the gastrointestinal tract

Kazunobu Tachibana, Seiichi Hirota, Hisashi Iizasa, Hisahiro Yoshida, Kenji Kawabata, Yuki Kataoka, Yukihiko Kitamura, Kouji Matsushima, Nobuaki Yoshida, Shin-ichi Nishikawa, Tadamitsu Kishimoto and Takashi Nagasawa ()
Additional contact information
Kazunobu Tachibana: Research Institute, Osaka Medical Center for Maternal and Child Health
Seiichi Hirota: Osaka University Medical School
Hisashi Iizasa: Research Institute, Osaka Medical Center for Maternal and Child Health
Hisahiro Yoshida: Faculty of Medicine, Kyoto University
Kenji Kawabata: Research Institute, Osaka Medical Center for Maternal and Child Health
Yuki Kataoka: Research Institute, Osaka Medical Center for Maternal and Child Health
Yukihiko Kitamura: Osaka University Medical School
Kouji Matsushima: Graduate School of Medicine, University of Tokyo
Nobuaki Yoshida: Research Institute, Osaka Medical Center for Maternal and Child Health
Shin-ichi Nishikawa: Faculty of Medicine, Kyoto University
Tadamitsu Kishimoto: Osaka University Medical School
Takashi Nagasawa: Research Institute, Osaka Medical Center for Maternal and Child Health

Nature, 1998, vol. 393, issue 6685, 591-594

Abstract: Abstract Vascularization of organs generally occurs by remodelling of the preexisting vascular system during their differentiation and growth to enable them to perform their specific functions during development. The molecules required by early vascular systems, many of which are receptor tyrosine kinases and their ligands, have been defined by analysis of mutant mice1,2,3. As most of these mice die during early gestation before many of their organs have developed, the molecules responsible for vascularization during organogenesis have not been identified. The cell-surface receptor CXCR4 (4–6) is a seven-transmembrane-spanning, G-protein-coupled receptor for the CXC chemokine PBSF/SDF-1 (for pre-B-cell growth-stimulating factor/stromal-cell-derived factor), which is responsible for B-cell lymphopoiesis, bone-marrow myelopoiesis and cardiac ventricular septum formation7. CXCR4 also functions as a co-receptor for T-cell-line tropic human immunodeficiency virus HIV-1 (ref. 8). Here we report that CXCR4 is expressed in developing vascular endothelial cells, and that mice lacking CXCR4 or PBSF/SDF-1 have defective formation of the large vessels supplying the gastrointestinal tract. In addition, mice lacking CXCR4 die in utero and are defective in vascular development, haematopoiesis and cardiogenesis, like mice lacking PBSF/SDF-1, indicating that CXCR4 is a primary physiological receptor for PBSF/SDF-1. We conclude that PBSF/SDF-1 and CXCR4 define a new signalling system for organ vascularization.

Date: 1998
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DOI: 10.1038/31261

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