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The Role of p38 Mitogen-Activated Protein Kinase in Hypoxia-Induced Vascular Cell Proliferation*: An Interspecies Comparison

David Welsh, PhD; Heather Mortimer, MD; Alan Kirk, MD; Andrew Peacock, MD
Author and Funding Information

*From the Scottish Pulmonary Vascular Unit (Drs. Welsh, Mortimer, and Peacock), Department of Surgery (Dr. Kirk), Western Infirmary, Glasgow, Scotland, UK.

Correspondence to: David Welsh, MD, Scottish Pulmonary Vascular Unit, Department of Surgery, Western Infirmary, Glasgow, Scotland, UK, G11 6NT; e-mail: david.welsh@bio.gla.ac.uk



Chest. 2005;128(6_suppl):573S-574S. doi:10.1378/chest.128.6_suppl.573S
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Extract

Physiologic and biochemical mechanisms that are activated by hypoxia exist in all animal species. Acute hypoxic exposure causes pulmonary artery vasoconstriction, which, if maintained, results in pulmonary artery remodeling. In contrast, systemic arteries vasodilate and do not remodel. Previously, work from our laboratory has demonstrated that p38 mitogen-activated protein (MAP) kinase phosphorylation is required for the hypoxia-induced proliferation of pulmonary, but not systemic, artery fibroblasts in both rat and bovine models.12

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