Potential Role for Antiangiogenic Proteins in the Evolution of Bronchopulmonary Dysplasia

Maria Lyn Quintos-Alagheband, Carl W. White, Margaret A. Schwarz

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

Impaired neovascularization is associated with the pathologic presentation of bronchopulmonary dysplasia (BPD). To determine if neovascularization and factors that negatively influence blood vessel formation play a role in the evolution of BPD, we examined the temporospatial distribution of a protein known to inhibit fetal lung neovascularization with associated dysplastic lung formation, endothelial-monocyte activating polypeptide (EMAP) II. Immunohistochemical analysis of EMAP II in lung tissues of human infants with BPD indicated an elevation in EMAP II abundance as compared with control. Utilizing a baboon model, western analysis indicated that EMAP II was increased twofold in those baboons with pathologic signs of BPD as compared with gestational controls. Consistent with our findings in human tissues, immunohistochemistry and in situ hybridization demonstrate that EMAP II is highly expressed in the perivascular stroma and dysplastic lung periphery in neonatal baboons with BPD as compared with controls. Lastly, there is a premature acceleration in EMAP II's perivascular distribution in term newborn baboon as compared with gestational control. The marked increase in EMAP II's temporal expression, its distribution in the perivascular and dysplastic alveolar regions of the lungs, and the interruption in vasculogenesis in BPD suggest that neovascularization and factors that negatively influence blood vessel formation may play a role in BPD evolution.

Original languageEnglish (US)
Pages (from-to)137-145
Number of pages9
JournalAntioxidants and Redox Signaling
Volume6
Issue number1
DOIs
StatePublished - Feb 2004

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

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