Features | Partner Sites | Information | LinkXpress
Sign In
GLOBETECH PUBLISHING LLC
PURITAN MEDICAL
Demo Company

Newly Developed Compound Protects Heart Cells During and After Infarction

By BiotechDaily International staff writers
Posted on 18 Feb 2013
Using two recently developed diverse compounds, scientists have been able to show in animal models that suppressing a specific enzyme protects heart cells and neighboring tissue against the debilitating injury incurred by heart attacks. The compounds also protect against additional damage from restored blood flow after an attack, a process known as reperfusion.

The study, which was led by Dr. Philip LoGrasso, a professor and senior scientific director of discovery biology at the Florida campus of The Scripps Research Institute (TSRI; Jupiter, USA), was published in the February 8, 2013, print edition of the Journal of Biological Chemistry.

A myocardial infarction greatly restricts blood supply, starving heart cells and neighboring tissue of oxygen, which can cause enormous damage in comparatively little time—at times in just a few minutes. This decrease in oxygen, known as an ischemic cascade, results in a sudden crush of metabolic waste that damages cell membranes as well as the mitochondria.

Restoring blood flow adds considerably to the damage, unfortunately, a serious medical issue when it comes to treating major ischemic events such as stroke and heart attack. Reperfusion triggers generation of free radicals and reactive oxygen species that attack and damage cells, intensifying inflammation, signaling white blood cells to attack otherwise salvageable cells and maybe even stimulating potentially lethal cardiac arrhythmias.

The new study revealed that inhibiting the enzyme, c-jun-N-terminal kinase (JNK; pronounced junk), protected against ischemic/reperfusion injury in lab rodents, reducing the total volume of tissue death by as much as 34%. It also substantially decreased levels of reactive oxygen species and mitochondrial dysfunction.

In earlier studies, TSRI scientists discovered that JNK migrates to the mitochondria upon oxidative stress. That migration, combined with JNK activation, they found, is associated with a number of severe health issues, including liver damage, neuronal cell death, stroke, and heart attack. The peptide and small molecule inhibitor (SR3306), developed by Dr. LoGrasso and his colleagues, blocks those harmful effects, thereby reducing programmed cell death four-fold.

“This is the same story,” said Dr. LoGrasso. “These just happen to be heart cells, but we know that oxidative stress kills cells, and JNK inhibition protects against this stress. Blocking the translocation of JNK to the mitochondria is essential for stopping this killing cascade and may be an effective treatment for damage done to heart cells during an ischemic/reperfusion event.”

Moreover, according to Dr. LoGrasso, biomarkers that intensify during a heart attack decrease in the presence of JNK inhibition, a distinct indication that blocking JNK reduces the severity of the infarction.

Related Links:

The Scripps Research Institute




Channels

Lab Technologies

view channel
Image: The Synergy Neo2 Multi-Mode Reader recently received Cisbio HTRF certification (Photo courtesy of BioTek Instruments Inc.).

High-Speed Multimode Microplate Reader Receives Homogenous Time-Resolved Fluorescence Certification

A new high-performance, high-speed microplate reader has received HTRF (homogenous time-resolved fluorescence) accreditation that certifies that it complies with standards for detection set by a major... Read more

Business

view channel

MS Drug Deal to Net More Than USD 1 Billion

A pharmaceutical company based in Switzerland has purchased the remaining rights to the multiple sclerosis drug Ofatumumab, which will allow it to continue development of the compound for treating relapsing remitting multiple sclerosis (RRMS) and similar autoimmune diseases. Novartis (Basel, Switzerland) recently announced... Read more
 
Copyright © 2000-2015 Globetech Media. All rights reserved.