Involvement of the Reck tumor suppressor protein in maternal and embryonic vascular remodeling in mice

Ediriweera Ps Chandana, Yasuhiro Maeda, Akihiko Ueda, Hiroshi Kiyonari, Naoko Oshima, Mako Yamamoto, Shunya Kondo, Junseo Oh, Rei Takahashi, Yoko Yoshida, Satoshi Kawashima, David B. Alexander, Hitoshi Kitayama, Chiaki Takahashi, Yasuhiko Tabata, Tomoko Matsuzaki, Makoto Noda

Research output: Contribution to journalArticlepeer-review

42 Citations (Scopus)


Background. Developmental angiogenesis proceeds through multiple morphogenetic events including sprouting, intussusception, and pruning. Mice lacking the membrane-anchored metalloproteinase regulator Reck die in utero around embryonic day 10.5 with halted vascular development; however, the mechanisms by which this phenotype arises remain unclear. Results. We found that Reck is abundantly expressed in the cells associated with blood vessels undergoing angiogenesis or remodelling in the uteri of pregnant female mice. Some of the Reck-positive vessels show morphological features consistent with non-sprouting angiogenesis. Treatment with a vector expressing a small hairpin RNA against Reck severely disrupts the formation of blood vessels with a compact, round lumen. Similar defects were found in the vasculature of Reck-deficient or Reck conditional knockout embryos. Conclusions. Our findings implicate Reck in vascular remodeling, possibly through non-sprouting angiogenesis, in both maternal and embyornic tissues.

Original languageEnglish
Article number84
JournalBMC Developmental Biology
Publication statusPublished - 2010

Bibliographical note

Funding Information:
We are grateful to Dr. Shin-ichi Nishikawa for his supports to EPSC in the early part of this study and to Shigeyoshi Itohara, Kazuki Nakao, and Shin-ichi Aizawa for their advice and help in generating Reck mutant mice. We also thank Dr. Masaaki Imamura for preparing cationized gelatin beads, Aiko Nishimoto, Hai-Ou Gu, and Mari Kojima for technical assistance, Aki Miyazaki for secretarial assistance, and all members of the laboratories for their help and advice. This work was supported by JSPS Grant-in-Aid for Creative Scientific Research and MEXT Grant-in-Aid on Priority Areas.

ASJC Scopus subject areas

  • Developmental Biology


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