Features Partner Sites Information LinkXpress
Sign In
Advertise with Us
RANDOX LABORATORIES

Events

06 Jun 2016 - 09 Jun 2016
22 Jun 2016 - 24 Jun 2016
04 Jul 2016 - 06 Jul 2016

Newly Developed Compound Protects Heart Cells During and After Infarction

By BiotechDaily International staff writers
Posted on 18 Feb 2013
Print article
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




Print article

Channels

Genomics/Proteomics

view channel
Image: Follicular helper T-cells (TFH cells, shown in blue) play a crucial role in the maturation of antibody-producing B-cells (shown in green). Activated B-cells give rise germinal centers (shown in red), where mature B-cells proliferate and produce highly specific antibodies against pathogens. Top left: normal germinal center in a mouse tonsil. All others: Germinal centers fail to form when the interaction between ICOS and TBK1 is interrupted (Photo courtesy of Dr. Kok-Fai Kong, La Jolla Institute for Allergy and Immunology).

Molecular Pathway Controlling High-affinity Antibody Production Identified

A molecular pathway has been identified that controls formation of follicular helper T-cells (TFH cells) germinal centers and production of high-affinity antibodies through interaction with the inducible... Read more

Drug Discovery

view channel

Experimental Small-Molecule Anticancer Drug Blocks RAS-binding Domains

The experimental small-molecule anticancer drug rigosertib was shown to block tumor growth by acting as an RAS-mimetic and interacting with the RAS binding domains of RAF kinases, resulting in their inability to bind to RAS, which inhibited the RAS-RAF-MEK pathway. Oncogenic activation of RAS genes due to point mutations... Read more

Biochemistry

view channel
Image: A space-filling model of the anticonvulsant drug carbamazepine (Photo courtesy of Wikimedia Commons).

Wastewater May Contaminate Crops with Potentially Dangerous Pharmaceuticals

Reclaimed wastewater used to irrigate crops is contaminated with pharmaceutical residues that can be detected in the urine of those who consumed such produce. Investigators at the Hebrew University... Read more

Lab Technologies

view channel

Huge Modifiable Biomedical Database to Be Available on the Wikidata Site

Genome researchers are exploiting the power of the open Internet community Wikipedia database to create a comprehensive resource for geneticists, molecular biologists, and other interested life scientists. While efficiency in generating scientific data improves almost daily, applying meaningful relationships between... Read more

Business

view channel

European Biotech Agreement to Promote Antigen-Drug Conjugation Technology

Two European biotech companies have joined forces to exploit and commercialize an innovative, site-specific ADC (antigen-drug conjugate) conjugation technology. ProBioGen (Berlin, Germany), a company specializing in the development and manufacture of complex glycoproteins and Eucodis Bioscience (Vienna, Austria), a... Read more
Copyright © 2000-2016 Globetech Media. All rights reserved.