@article{ref1,
title="Myeloperoxidase increased cardiomyocyte protein nitration in mice subjected to nonlethal mechanical trauma",
journal="Biochemical and biophysical research communications",
year="2010",
author="Yan, Zi and Liang, Feng and Guo, Lijuan and Wang, Jiangping and Wang, Xiao-Liang and Cheng, Xiao-Long and Ma, Xin L. and Liu, Hui-Rong",
volume="393",
number="3",
pages="531-535",
abstract="Nonlethal mechanical trauma causes cardiomyocyte apoptosis which contributes to posttraumatic cardiac dysfunction. Apoptosis is positively correlated with protein nitration in the traumatic heart. However, the mechanisms responsible for the cardiomyocyte protein nitration remain unclear. The present study was designed to identify whether myeloperoxidase may contribute to protein nitration in nonlethal mechanical trauma and subsequent cardiomyocyte apoptosis, and, if so, to determine the possible mechanisms responsible. We used Noble-Collip drum to make nonlethal traumatic mice models. Male adult C57B16/J mice were placed in the Noble-Collip drum and subjected to a total of 200 revolutions at a rate of 40r/min. Then myeloperoxidase activity and release, protein nitration, cardiomyocyte apoptosis, endothelial function and intercellular adhesion molecule-1 expression were determined. Nonlethal mechanical trauma was characterized by the 100% survival rate during the first 24 hours after trauma, the lack of circulatory shock and without direct heart injury. However, myeloperoxidase activity significantly increased 6 hours after trauma, and reached a maximum level 12 hours after trauma. Obviously, protein nitration and cardiomyocyte apoptosis increased 12 hours after trauma and could be blocked by administration of R15.7, a monoclonal antibody that blocks polymorphonuclear neutrophils adhesion. Moreover, endothelial dysfunction and intercellular adhesion molecule-1 upregulation were observed in traumatic mice. Our present study demonstrated for the first time that myeloperoxidase caused protein nitration and cardiomyocyte apoptosis in nonlethal traumatic mice. Inhibition of polymorphonuclear neutrophils adhesion and antinitration treatments may be novel measures in reducing posttraumatic cardiomyocyte apoptosis and secondary heart injury.<p /> <p>Language: en</p>",
language="en",
issn="0006-291X",
doi="10.1016/j.bbrc.2010.02.049",
url="http://dx.doi.org/10.1016/j.bbrc.2010.02.049"
}