19
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Overexpression of placenta growth factor contributes to the pathogenesis of pulmonary emphysema.

      American journal of respiratory and critical care medicine
      Animals, Antigens, CD31, metabolism, Apoptosis, physiology, Cell Division, Cell Line, Dose-Response Relationship, Drug, Extracellular Matrix Proteins, Growth Substances, Image Processing, Computer-Assisted, In Situ Nick-End Labeling, Lung, cytology, drug effects, pathology, Mice, Mice, Transgenic, Myosin Heavy Chains, Nonmuscle Myosin Type IIB, Pregnancy Proteins, biosynthesis, pharmacology, Pulmonary Alveoli, growth & development, Pulmonary Emphysema, physiopathology, Reverse Transcriptase Polymerase Chain Reaction, Vascular Endothelial Growth Factor A

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          To examine the role of placenta growth factor (PlGF) in the pathogenesis of pulmonary emphysema, we generated PlGF-transgenic (TG) mice using a phosphoglycerate kinase promoter. This resulted in constitutive overexpression of PlGF. In these TG mice, pulmonary emphysema, with enlarged air spaces and enhanced pulmonary compliance, first appeared at 6 months of age and became prominent at 12 months. Increased alveolar septal cell apoptosis was noted in their lungs. Fluorescence-activated cell sorter analysis suggests that these apoptotic septal cells are type II pneumocytes. At the same time, the messenger RNA of vascular endothelial growth factor and platelet-endothelial cell adhesion molecule-1, an endothelial cell marker, were downregulated indicating a reduced number of endothelial cells and its survival factor VEGF. In vitro, exogenous PlGF can inhibit the proliferation and promote the cell death of mouse type II pneumocytes. In normal newborn mice, abundant expression of PlGF messenger RNA was detected in the lungs during saccular division but was rapidly downregulated after alveolarization was complete. Thus, a persistently elevated PlGF was detrimental to the developed lung and causes the emphysematous change seen in our TG mice. Our study suggests that PlGF plays an important role in the pathogenesis of pulmonary emphysema via its action on type II pneumocytes.

          Related collections

          Author and article information

          Comments

          Comment on this article