Abstract | BACKGROUND: METHODS: RESULTS: After 4 weeks of PPE instillation, lung airspaces enlarged more significantly in WT than in KO mice. The levels of TNF-alpha and MMP-9, but not VEGF, increased in the lungs of WT compared with those of KO mice. There was also increased in apoptosis of alveolar septal cells in WT mice. Instillation of exogenous PlGF in KO mice restored the emphysematous changes. The expression of both VEGF R1 and R2 decreased in the emphysematous lungs. CONCLUSION: In this animal model, pulmonary emphysema is prevented by depleting PlGF. When exogenous PlGF is administered to PlGF KO mice, emphysema re-develops, implying that PlGF contributes to the pathogenesis of emphysema.
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Authors | Shih Lung Cheng, Hao Chien Wang, Chong Jen Yu, Po Nien Tsao, Peter Carmeliet, Shi Jung Cheng, Pan Chyr Yang |
Journal | Respiratory research
(Respir Res)
Vol. 10
Pg. 115
(Nov 23 2009)
ISSN: 1465-993X [Electronic] England |
PMID | 19930612
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- PGF protein, human
- Pgf protein, mouse
- Pregnancy Proteins
- Tumor Necrosis Factor-alpha
- Vascular Endothelial Growth Factor A
- vascular endothelial growth factor A, mouse
- Placenta Growth Factor
- Vascular Endothelial Growth Factor Receptor-1
- Vascular Endothelial Growth Factor Receptor-2
- Pancreatic Elastase
- Matrix Metalloproteinase 9
- Mmp9 protein, mouse
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Topics |
- Animals
- Apoptosis
- Disease Models, Animal
- Lung
(metabolism, pathology)
- Matrix Metalloproteinase 9
(metabolism)
- Mice
- Mice, Knockout
- Pancreatic Elastase
- Placenta Growth Factor
- Pregnancy Proteins
(deficiency, genetics)
- Pulmonary Emphysema
(chemically induced, metabolism, pathology, prevention & control)
- Tumor Necrosis Factor-alpha
(metabolism)
- Vascular Endothelial Growth Factor A
(metabolism)
- Vascular Endothelial Growth Factor Receptor-1
(metabolism)
- Vascular Endothelial Growth Factor Receptor-2
(metabolism)
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