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New class of compounds stops disease-fueling inflammation in lab tests
Date:2/23/2012

lving Rac GTPases, a family of intracellular signal transducers that amplify ROS production by the NOX2 enzyme network.

Normally, Rac GTPases maintain cell growth and survival programs in the body, including the NOX enzyme network and its activation of ROS production in cells. When signaling miscues occur they cause an unusually high burst of ROS production and release harmful superoxide chemicals. This up-regulation creates excessive inflammation that damages tissues and drives the onset of diseases like Chronic Obstructive Pulmonary Disease, ischemia-induced lung and brain damage and hypertension, among others.

Previous attempts to create compounds that target and stop harmful ROS production, including an earlier compound developed by Dr. Zheng's laboratory, have been able to reduce inflammation in cells. Unfortunately, the compounds were not specific or efficient enough in targeting the Rac GTPase regulatory pathway. This meant the compounds inhibited several different cellular processes including some that are necessary and beneficial leading to toxicity.

Zheng and his colleagues achieved greater specificity and efficiency through their design of small molecular inhibitors they named Phox-I1 and Phox-I2. The inhibitors precisely target and block the binding of a signal sensor for the NOX2 enzyme called p67-phox to Rac GTPase. P67-phox has to bind with Rac GTPase to activate the oxidase enzyme complex of NOX2 (known as NADPH) that produces superoxide and causes inflammation.

In laboratory tests involving normal human blood cells, leukemic cells and mouse blood cells, Phox-l1blocked p67-phox binding with Rac. It did so in a dose-dependent manner with enough precision to shut down ROS production without causing unwanted toxicity in the cells, the researchers report. In unpublished test results on mouse models of lung inflammation, Zheng said the investigators found that the Phox-I lead compounds are effective in blocking ne
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Contact: Nick Miller
nicholas.miller@cchmc.org
513-803-6035
Cincinnati Children's Hospital Medical Center
Source:Eurekalert

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