title: Expression of angiogenic factors and their receptors in postnatal mouse developing lung.
abstract: OBJECTIVE
  Several lines of evidence suggest that angiogenesis is necessary for alveolarization and that inhibition of vascular growth during a critical period of early growth may impair alveolarization. However, little is known about the role of angiogenic factors during alveolarization. This study investigated the expression patterns of the Ang-Tie-2 family of endothelium-specific receptor tyrosine kinases and vascular endothelial growth factors and their receptors (VEGF-VEGFR system) during postnatal mouse lung development.
  
  
  METHODS
  The lungs from 3 or 4 mice from groups aged 3, 7, 10 and 14 days and adults were removed and dissected from the main bronchi for reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. Semi-quantitative RT-PCR of mouse lung total RNA was used to measure the expression levels of these angiogenic factors and their receptors.
  
  
  RESULTS
  During alveolarization, VEGF/Flk-1, Ang-1, Ang-2, and Tie-2 were up-regulated and PlGF/Flt-1 was kept at a relatively constant level. After alveolarization was completed, PlGF was down-regulated, Flt-1 was up-regulated, and VEGF/Flk-1, Ang-1, Ang-2, and Tie-2 were maintained at relatively high levels.
  
  
  CONCLUSIONS
  During alveolarization, in mice, VEGF/Flk-1, Ang-1, Ang-2, and Tie-2 are up-regulated and PlGF/ Flt-1 is kept at relatively constant level to promote pulmonary microvascular development. In the adult mouse lung, when most of the vascular network is complete, PlGF is down-regulated and Flt-1 is up-regulated to stop angiogenesis and VEGF/Flk-1, Ang-1, Ang-2 and Tie-2 are kept at relatively high levels to maintain mature pulmonary microvasculature.
authors.affiliation: Division of Neonatology, Department of Pediatrics, National Taiwan University Hospital and Taiwan University College of Medicine, Taipei, Taiwan.
authors.forename: Po-Nien
authors.initials: PN
authors.lastname: Tsao
authors.forename: Hung
authors.initials: H
authors.lastname: Li
authors.forename: Shu-Chen
authors.initials: SC
authors.lastname: Wei
authors.forename: Min-Liang
authors.initials: ML
authors.lastname: Ko
authors.forename: Hung-Chieh
authors.initials: HC
authors.lastname: Chou
authors.forename: Wu-Shiun
authors.initials: WS
authors.lastname: Hsieh
authors.forename: Fon-Jou
authors.initials: FJ
authors.lastname: Hsieh
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D008168:Lung / Q000098:blood supply* / Q000378:metabolism*; D051379:Mice; D018919:Neovascularization, Physiologic / Q000502:physiology*; D000072483:Placenta Growth Factor; D011257:Pregnancy Proteins / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000378:metabolism*
chemical_list: C000608037:Pgf protein, mouse; D011257:Pregnancy Proteins; D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A; D000072483:Placenta Growth Factor; D020794:Receptor Protein-Tyrosine Kinases; D040301:Vascular Endothelial Growth Factor Receptor-2