Researchers turn to genes to reduce heart damageJune 23rd, 2008 - 1:17 pm ICT by IANS
Washington, June 23 (IANS) Researchers are looking at something as basic as genes to find ways to reduce or prevent heart damage. Keith Jones, a pharmacology researcher at Cincinnati University, is trying to reduce post-heart attack damage by studying the way cells die - a process controlled by transcription factors.
Transcription factors are proteins that bind to specific parts of DNA and are part of a system that controls the transfer of genetic information from DNA to RNA and then to protein.
Transfer of genetic information also plays a role in controlling the cycle of cells - from cell growth to cell death. “We call it ‘gene regulatory therapy,’” said Jones.
So far, studies have identified the role for an important group of interacting transcription factors and the genes they regulate to determine whether cells in the heart survive or die after blood flow restriction occurs.
Often, scientists use virus-like mechanisms to transfer DNA and other nucleic acids inside the body.
The “virus” takes over other healthy cells by injecting them with its DNA. The cells, then transformed, begin reproducing the virus’ DNA. Eventually they swell and burst, sending multiple replicas of the virus out to conquer other cells and repeat the process.
Now, the researchers are further investigating new, non-viral delivery mechanisms for this transfer of DNA.
“We can use non-viral delivery vehicles to transfer nucleic acids, including transcription factor decoys, to repress activation of specific transcription factors in the heart,” Jones said.
Researchers have made this successfully work within live animal models.
“This means we can block the activity of most transcription factors in the heart without having to make genetically engineered mice,” he added.
Jones presented these findings Sunday at the International Society for Heart Research in Cincinnati.
Tags: animal models, blood flow, cell death, cincinnati university, decoys, delivery mechanisms, delivery vehicles, flow restriction, genetic information, heart attack, heart attack damage, heart damage, heart research, nucleic acids, protein transfer, replicas, rna, transcription factor, transcription factors, virus dna