Involvement of the Reck tumor suppressor protein in maternal and embryonic vascular remodeling in mice.
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 embyonic tissues.
Chandana
Ediriweera P S
EP
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan.
Maeda
Yasuhiro
Y
Ueda
Akihiko
A
Kiyonari
Hiroshi
H
Oshima
Naoko
N
Yamamoto
Mako
M
Kondo
Shunya
S
Oh
Junseo
J
Takahashi
Rei
R
Yoshida
Yoko
Y
Kawashima
Satoshi
S
Alexander
David B
DB
Kitayama
Hitoshi
H
Takahashi
Chiaki
C
Tabata
Yasuhiko
Y
Matsuzaki
Tomoko
T
Noda
Makoto
M
D000818:Animals; D001808:Blood Vessels / Q000378:metabolism; D010064:Embryo Implantation; D004622:Embryo, Mammalian / Q000098:blood supply*; D005260:Female; D058851:GPI-Linked Proteins; D008562:Membrane Glycoproteins / Q000378:metabolism*; D051379:Mice; D018919:Neovascularization, Physiologic; D011247:Pregnancy; D014599:Uterus / Q000098:blood supply*
D058851:GPI-Linked Proteins; D008562:Membrane Glycoproteins; C492025:Reck protein, mouse