Lung Injury/Sepsis

Stephen M. Black is a medical researcher with Georgia Regents University in Atlanta, Georgia. A number of his co-authored articles about this research have been published in peer-reviewed medical research journals, including:


Lipopolysaccharide Induced Lung Injury Involves the Nitration-Mediated Activation of RhoA.

Acute lung injury is characterized by increased endothelial hyperpermeability. Stephen M. Black and the study’s other authors noted that protein nitration has been shown to be involved in LPS exposed mice in the endothelial barrier dysfunction but researchers had thus far been unable to identify which proteins specifically. This study resulted in identification of a new mechanism of nitration-mediated RhoA activation, which is involved in the LPS-mediated endothelial barrier dysfunction. Additionally, researchers were able to show the potential utility of “shielding” peptides in order to prevent RhoA nitration when managing acute lung injury. This study appeared in the February 21, 2014 Journal of Biological Chemistry.

Dimethylarginine Dimethylaminohydrolase II Over-Expression Attenuates Lipopolysaccharide Mediated Lung Leak in Acute Lung Injury.

Acute lung injury is associated with lung leak, inflammation, diffuse alveolar damage, and a loss of lung function. It has been shown that combining a decrease in DDAH and increase in ADMA in mice exposed to LPS can contribute to the development of acute lung injury. The study’s authors saw that DDAH II overexpression prevented LPS-dependent increases in ADMA with human lung microvascular endothelial cells. Additionally, they were able to demonstrate that targeted overexpression of DDAH II in vivo inhibited the accumulation of ADMA in the lungs of mice exposed to LPS. This data suggests that enhancing DDAH II activity could be a useful adjuvant therapy for treating patients with acute lung injury. This study appeared in the March 2014 issue of American Journal of Respiratory Cell Molecular Biology.


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