Abstract
The authors tested whether macrophage metalloelastase (MMP-12) and substance P (SP) were increased in the cigarette smoke (CS)-exposed female C3H/HeN mice with hypercapnic emphysema. The authors found that as compared to control (filtered air), 16 weeks of CS exposure significantly up-regulated mRNA and protein levels of MMP-12, the ratio of MMP-12/tissue inhibitor of matrix metalloproteinase-1, and SP/preprotachykinin-A (a precursor to SP) in the lungs. Importantly, a significant correlation was found between MMP-12 and SP, and between MMP-12/SP and the degrees of hypoxemia/hypercapnia denoted in CS-exposed mice. These data suggest a possible involvement of SP and MMP-12 in the pathogenesis of severe COPD.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Bronchoalveolar Lavage Fluid / cytology
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Carbon Dioxide / blood
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Female
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Gene Expression Regulation
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Hypercapnia / etiology*
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Hypoxia / etiology
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Lung / metabolism*
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Lung / pathology
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Macrophages, Alveolar / metabolism
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Macrophages, Alveolar / pathology
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Matrix Metalloproteinase 12 / genetics
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Matrix Metalloproteinase 12 / metabolism*
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Mice
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Mice, Inbred C3H
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Oxygen / blood
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Pulmonary Disease, Chronic Obstructive / metabolism
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Pulmonary Emphysema / etiology*
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Receptors, Neurokinin-1
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Substance P / genetics
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Substance P / metabolism*
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Tissue Inhibitor of Metalloproteinase-1 / genetics
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Tissue Inhibitor of Metalloproteinase-1 / metabolism
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Tobacco Smoke Pollution / adverse effects*
Substances
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RNA, Messenger
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Receptors, Neurokinin-1
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Tissue Inhibitor of Metalloproteinase-1
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Tobacco Smoke Pollution
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Carbon Dioxide
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Substance P
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Matrix Metalloproteinase 12
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Oxygen