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D61. ANIMAL MODELS OF PULMONARY ARTERIAL HYPERTENSION: NEW IDEAS AND INSIGHTS - Increased Lung MIF Expression in A Hypoxia Induced Pulmonary Hypertension Mice Model by Zhang, Yinzhong; Koga, Kiyokazu; Linge, Helena M.; Lin, Ke; Talwar, Arunabh; Miller, Edmund J. is a scholarly article available to read on EtoBox.

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Inflammatory mechanisms play an important role in the etiology of pulmonary hypertension (PH). Macrophage migration RATIONALE: inhibitory factor (MIF) is a proinflammatory cytokine and has been reported to increase cell proliferation in several models. Our previous studies indicate the lung is a major source of MIF, and that there is increased MIF in plasma from individuals with PH. In addition, our in studies suggest that MIF mediates hypoxia-driven lung fibroblast proliferation. Therefore, we reasoned that MIF may play an vitro important role in hypoxia-driven vascular remodeling and resultant pulmonary hypertension. We have studied the METHODS: elaboration of MIF in a murine model of hypoxia-induced pulmonary hypertension. C57BL6 mice (8-10 week old) were randomized into 4 groups, and housed in either normoxia (control, n=7) or 10% normobaric hypoxia for 3, 10, or 42 days (n=5/hypoxia group). At the end of the study period, right ventricular systolic pressure (RVSP) was measured, and blood sampled for plasma MIF assessment by Western blot analysis. Lung tissue was collected for qPCR quantitation of mRNA encoding MIF. The heart was also harvested, dissected and weighed to assess

Author

Zhang, Yinzhong; Koga, Kiyokazu; Linge, Helena M.; Lin, Ke; Talwar, Arunabh; Miller, Edmund J.

Publisher

American Thoracic Society

Published

2010

Language

EN