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Am J Physiol Lung Cell Mol Physiol 282: L26-L35, 2002; doi:10.1152/ajplung.00171.2001
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Vol. 282, Issue 1, L26-L35, January 2002

Altered hemodynamics controls matrix metalloproteinase activity and tenascin-C expression in neonatal pig lung

Peter Lloyd Jones1, Rene Chapados2, H. Scott Baldwin2, Gary W. Raff2, Eugene V. Vitvitsky2, Thomas L. Spray2, and J. William Gaynor2

1 Department of Pediatrics, University of Colorado Health Sciences Center, Denver, Colorado 80262; and 2 Department of Pediatrics, The Children's Hospital of Philadelphia and The University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-4399

Tenascin-C (TN-C) expression and matrix metalloproteinase (MMP) activity are induced within remodeling pulmonary arteries (PAs), where they promote cell growth. Because pulmonary vascular disease in children with congenital heart defects is commonly associated with changes in pulmonary hemodynamics, we hypothesized that changes in pulmonary blood flow regulate TN-C and MMPs. To test this, we ligated the left PAs of neonatal pigs. After 12 wk, we evaluated the levels of TN-C and MMPs in control and ligated lung tissue. Modifying pulmonary hemodynamics increased TN-C mRNA and protein expression, MMP activity, and the DNA-binding activity of Egr-1, a transcription factor that has been shown to activate TN-C expression. To link MMP-mediated remodeling of the extracellular matrix to increased TN-C expression and Egr-1 activity, porcine PA smooth muscle cells were cultivated either on denatured type I collagen, which supported TN-C expression and Egr-1 activity, or on native collagen, which had the opposite effect. These data provide a framework for understanding how changes in pulmonary blood flow in the neonate modify the tissue microenvironment and cell behavior.

pulmonary vascular disease; Egr-1


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