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Researchers work to take the pressure off newborns' lungs
Date:7/27/2011

as the byproduct citrulline which interacts with two enzymes that convert it back to arginine, repeating the process anew. Sharma's early findings show that high pressures from the heart defect disrupts the cell's powerhouse, or mitochondria. That means insufficient amounts of the energy source ATP are produced, hindering the function of the molecular chaperone, HSP90, which helps the enzymes do their job.

"Upstream you can see one thing getting disrupted and downstream all the molecules it's regulating are affected," Sharma said.

That's where PPAR agonists come in. Dr. Stephen Black, a cell and molecular physiologist at the Vascular Biology Center who co-directs the Cardiovascular Discovery Institute, has shown that PPAR signaling falters in their animal model of pulmonary hypertension, impairing the cell powerhouse. In fact by blocking PPAR signaling, the researchers have produced the negative effects on the blood vessels without the heart defect.

"We hope that adding a PPAR agonist will improve mitochondrial activity and function and downstream help improve arginine recycling and nitric oxide production," Sharma said. She is retracing the recycling process to see how the agonist impacts each known step as well as the desired bottom line of improved nitric oxide production. "We're optimistic that we can get these two enzymes back to doing what they are supposed to."


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Contact: Toni Baker
tbaker@georgiahealth.edu
706-721-4421
Georgia Health Sciences University
Source:Eurekalert  

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