TY - JOUR
T1 - Involvement of the Reck tumor suppressor protein in maternal and embryonic vascular remodeling in mice
AU - Chandana, Ediriweera Ps
AU - Maeda, Yasuhiro
AU - Ueda, Akihiko
AU - Kiyonari, Hiroshi
AU - Oshima, Naoko
AU - Yamamoto, Mako
AU - Kondo, Shunya
AU - Oh, Junseo
AU - Takahashi, Rei
AU - Yoshida, Yoko
AU - Kawashima, Satoshi
AU - Alexander, David B.
AU - Kitayama, Hitoshi
AU - Takahashi, Chiaki
AU - Tabata, Yasuhiko
AU - Matsuzaki, Tomoko
AU - Noda, Makoto
N1 - 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.
PY - 2010
Y1 - 2010
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=77955188882&partnerID=8YFLogxK
U2 - 10.1186/1471-213X-10-84
DO - 10.1186/1471-213X-10-84
M3 - Article
C2 - 20691046
AN - SCOPUS:77955188882
VL - 10
JO - BMC Developmental Biology
JF - BMC Developmental Biology
SN - 1471-213X
M1 - 84
ER -