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Articles in PresS, published online ahead of print November 27, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00290.2002
Submitted on August 22, 2002
Accepted on November 25, 2002
1 Department of Medicine and Research, VAMC Northport, Northport, NY, USA; Department of Medicine, State University of New York at Stony Brook, Stony Brook, NY, USA
* To whom correspondence should be addressed. E-mail: hfoda{at}mail.som.sunysb.edu.
High volume mechanical ventilation leads to ventilator induced lung injury (VILI). This type of lung injury is accompanied by an increased release and activation of matrix metalloproteinases (MMPs). To investigate the mechanism leading to the increased MMP release, we systematically studied the effect of mechanical stretch on human microvascular endothelial cells isolated from lung (HMVEC-L). Cells grown on collagen 1 BioFlex ® plates were exposed to sinusoidal cyclic stretch at 0.5 Hz using the FlexerCell ® system with 17-18% elongation of cells. After 4 days of cell stretching, conditioned media and cell lysate were collected and analyzed by gelatin, casein, and reverse zymograms as well as Western blotting. RT-PCR of mRNA extracted from stretched cells was performed. Our results show that: 1) cyclic stretch led to an increased release and activation of MMP-2 and MMP-1; 2) The activation of MMP-2 was accompanied by an increase in membrane type 1-MMP (MT1-MMP) and inhibited by a hydroxamic acid derived inhibitor of MMPs (Prinomastat: AG3340); and 3) the MMP-2 release and activation was preceded by an increase in production of extracellular MMP inducer (EMMPRIN). These results suggest that cyclic mechanical stretch leads to MMP-2 activation through a MT1-MMP mechanism. EMMPRIN may play an important role in the release and activation of MMPs during lung injury.
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