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1 Developmental Biology and Cardiothoracic Surgery Program, Childrens Hospital Research Institute of Los Angeles, Los Angeles, California 90027; and 2 Department of Physiology and Cellular Biophysics, Columbia University, New York, New York 10032
Neovascularization
is a key regulatory process in fetal growth and development. Although
factors promoting growth and development of the pulmonary vasculature
have been investigated, nothing is known regarding the molecular
mechanisms that may counteract these stimuli. Endothelial
monocyte-activating polypeptide (EMAP) II has recently been identified
as an antiangiogenic factor in tumor vascular development. We
postulated that EMAP II is a putative negative modulator of lung
vascular growth. EMAP II mRNA and protein decrease fivefold
(P < 0.01) as the developing lungs
in the fetal mouse progress from having poor vascularization
(day
14) to having complete vascular
development at term (day
18.5). EMAP II protein expression continues to remain low throughout postnatal life and into
adulthood, with the exception of a surge that correlates with
microvascular maturation. Furthermore, through the use of in situ
hybridization and immunohistochemistry, EMAP II is localized throughout
the lung, with significant expression in the
submyoepithelial area during the early stages of lung
development when there is minimal vascular development. In contrast,
EMAP II is distributed around the large vessels during the end of
vascular development, suggesting that EMAP II modulates the
neovascularization process. We speculate that EMAP II is a director of
neovascularization in the developing lung.
pulmonary; fetal; vasculogenesis; angiogenesis; antiangiogenesis
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