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Up-regulation of Angiogenic Factor Expression in Hypoxia-Treated Mouse Lung Demonstrated By DNA Array Technique*

Dechun Li, MD, PhD; Xingwu Teng, MD, PhD; Roger A. Johns, MD
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*From the Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.

Correspondence to: Roger A. Johns, MD, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, 600 N Wolfe St, Blalock 1415, Baltimore, MD 21287-4965



Chest. 2002;121(3_suppl):78S. doi:10.1378/chest.121.3_suppl.78S
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Hypoxia can induce pulmonary vasoconstriction and pulmonary hypertension. Increased vascular endothelial cell proliferation and muscularization of the vasculature are the pathologic characteristics of pulmonary vascular remodeling, and it has been demonstrated that this process is mediated by the increased production of angiogenic factors and vasoconstrictors to hypoxia. In this study, adult male mice were exposed to 10% O2 for 4 days, and the cell proliferation of the pulmonary vasculature was determined by proliferating cell nuclear antigen staining. RNAs from the lungs of normoxia-treated and hypoxia-treated mice were extracted, converted into complementary DNA, and labeled with 32P. The labeled complementary DNA probes were hybridized with mouse angiogenesis-1 DNA array membranes. After exposure, the images were scanned (Storm PhosphorImager; Molecular Dynamics; Sunnyvale, CA) and quantitated (ImageQuant; Molecular Dynamics). The results demonstrated that there was a significant increase of proliferating cell nuclear antigen labeling indexes in the hypoxia-treated pulmonary vasculature (p < 0.02 [t test compared to normoxic group]). In addition, hypoxia up-regulated several angiogenic factors, including angiopoietin-2 (1.4-fold increase), platelet-derived growth factor-A (1.5-fold increase), vascular endothelial growth factor-C (2.5-fold increase), and vascular endothelial growth factor-D (1.8-fold increase compared to normoxia-treated animals). These results indicate that hypoxia-induced cell proliferation in the pulmonary vasculature may be a consequence of the altered expression of angiogenic factors. The increased level of angiogenic factors due to hypoxia may play important roles in the control and mediation of the proliferation of vascular endothelial cells and smooth muscle cells. An understanding of the angiogenic factor gene expression profile may lead to a way to find new methods for the prevention and treatment of hypoxia-induced pulmonary hypertension.

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