PMID- 20172951
OWN - NLM
STAT- MEDLINE
DCOM- 20110726
LR  - 20211020
IS  - 1522-1504 (Electronic)
IS  - 1040-0605 (Print)
IS  - 1040-0605 (Linking)
VI  - 298
IP  - 5
DP  - 2010 May
TI  - Chorioamnionitis stimulates angiogenesis in saccular stage fetal lungs via CC 
      chemokines.
PG  - L637-45
LID - 10.1152/ajplung.00414.2009 [doi]
AB  - The fetal lung vasculature forms in tandem with developing airways. Whereas 
      saccular airway morphogenesis is arrested in bronchopulmonary dysplasia (BPD), 
      the potential vascular phenotype in BPD at this stage of development is less 
      well-understood. As inflammation increases the risk of BPD and induces arrest of 
      saccular airway morphogenesis, we tested the effects of Escherichia coli LPS on 
      fetal mouse lung vascular development. Injecting LPS into the amniotic fluid of 
      Tie2-lacZ endothelial reporter mice at embryonic day 15 stimulated angiogenesis 
      in the saccular stage fetal lung mesenchyme. LPS also increased the number of 
      endothelial cells in saccular stage fetal mouse lung explants. Inflammation 
      appeared to directly promote vascular development, as LPS stimulated pulmonary 
      microvascular endothelial cell angiogenesis, cell migration, and proliferation in 
      vitro. Whereas LPS did not increase expression of VEGF, angiopoietin-1 (Ang-1), 
      Tie2, fetal liver kinase-1 (Flk-1), fms-like tyrosine kinase-1 (Flt-1), PDGFA, 
      PDGFB, heparin-binding EGF-like growth factor (HB-EGF), or connective tissue 
      growth factor (CTGF), LPS did stimulate the production of the angiogenic CC 
      chemokines macrophage inflammatory protein-1alpha (MIP-1alpha) and monocyte 
      chemoattractant protein-1 (MCP-1). Both MIP-1alpha and MCP-1 increased angiogenesis 
      in fetal mouse lung explants. In addition, inhibitory antibodies against MIP-1alpha 
      and MCP-1 blocked the effects of LPS on fetal lung vascular development, 
      suggesting these chemokines are downstream mediators of LPS-induced angiogenesis. 
      We speculate that an inflammation-mediated surge in angiogenesis could lead to 
      formation of aberrant alveolar capillaries in the lungs of patients developing 
      BPD.
FAU - Miller, J Davin
AU  - Miller JD
AD  - Departments of Pediatrics, Monroe Carell Jr. Children's Hospital at Vanderbilt, 
      Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
FAU - Benjamin, John T
AU  - Benjamin JT
FAU - Kelly, David R
AU  - Kelly DR
FAU - Frank, David B
AU  - Frank DB
FAU - Prince, Lawrence S
AU  - Prince LS
LA  - eng
GR  - R01 HL086324/HL/NHLBI NIH HHS/United States
GR  - R01 HL097195/HL/NHLBI NIH HHS/United States
GR  - HL-086324/HL/NHLBI NIH HHS/United States
GR  - HL-097195/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20100219
PL  - United States
TA  - Am J Physiol Lung Cell Mol Physiol
JT  - American journal of physiology. Lung cellular and molecular physiology
JID - 100901229
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Ccl3 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Chemokines, CC)
RN  - 0 (Lipopolysaccharides)
SB  - IM
MH  - Animals
MH  - Bronchopulmonary Dysplasia/embryology/etiology/immunology
MH  - Case-Control Studies
MH  - Chemokine CCL2/antagonists & inhibitors/pharmacology
MH  - Chemokine CCL3/antagonists & inhibitors/pharmacology
MH  - Chemokines, CC/*metabolism
MH  - Chorioamnionitis/*immunology
MH  - Disease Models, Animal
MH  - Endothelial Cells/drug effects/physiology
MH  - Female
MH  - Humans
MH  - Immunity, Innate
MH  - Infant
MH  - Infant, Newborn
MH  - Lipopolysaccharides/pharmacology
MH  - Lung/abnormalities/*blood supply/*embryology/immunology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Transgenic
MH  - *Neovascularization, Physiologic/drug effects/immunology
MH  - Pregnancy
PMC - PMC2867403
EDAT- 2010/02/23 06:00
MHDA- 2011/07/27 06:00
PMCR- 2011/05/01
CRDT- 2010/02/23 06:00
PHST- 2010/02/23 06:00 [entrez]
PHST- 2010/02/23 06:00 [pubmed]
PHST- 2011/07/27 06:00 [medline]
PHST- 2011/05/01 00:00 [pmc-release]
AID - 00414.2009 [pii]
AID - L-00414-2009 [pii]
AID - 10.1152/ajplung.00414.2009 [doi]
PST - ppublish
SO  - Am J Physiol Lung Cell Mol Physiol. 2010 May;298(5):L637-45. doi: 
      10.1152/ajplung.00414.2009. Epub 2010 Feb 19.