Gene Response Following Myocardial Infarction
In the most comprehensive study of its kind, researchers at Allegheny General Hospital in Pittsburgh, Pennsylvania using GE Healthcare’s CodeLink have gathered significant data shedding new light on the important gene expression changes that occur in the heart following myocardial infarction (MI). Data gathered from this study were published in the January issue of the Journal of Molecular and Cellular Cardiology.
“The results of this study raise the possibility of developing revolutionary new treatments to minimize the impact of MI. Understanding in more detail the complex pattern of the changes activated by myocardial injury will allow the medical community to develop therapies that may preserve heart muscle before it deteriorates,” said Dr. Robert Guthrie, Director, Division of Neonatology, Allegheny General Hospital and Professor of Pediatrics, Drexel University School of Medicine. “A key component in our research was the CodeLink system, which allowed us to advance previous research through its highly sensitive microarrays and improved techniques for detecting slight yet critical changes in gene expression. Importantly, CodeLink was technically precise, but did not burden our research with complex informatics, making the data easier for us to understand and interpret internally.”
A major finding of the study was that genes affected by a MI are not deactivated; rather they attempt to repair and rejuvenate in the area of the heart that was affected. Myocardial infarction, also known as a heart attack, occurs when the blood supply to part of the heart muscle itself — the myocardium — is severely reduced or stopped. If the blood supply is cut off for more than a few minutes, muscle cells suffer permanent injury and die. This can kill or disable someone, depending on how much heart muscle is damaged. Cardiovascular disease (CVD) is the number one killer in the United States. Of the 64,400,000 Americans with one or more types of CVD, approximately 7,800,000 experience MI.
This preclinical study was undertaken to outline the multiple molecular processes that occur in the heart following a MI. Successful MI compensation involved early remote zone gene activation including an acute phase response, initiation of a cytoprotective program, recruitment of extensive developmental transcription factors and induction of signaling pathways associated with cell proliferation. Despite overriding transcriptional depression, the infarct zone exhibited an early cytoprotective response through recruitment of different gene families than the remote zone. By Day 28, the infarct zone adopted a strategy mirroring the early remote zone including expression of developmental transcription factors, proliferation signals, and matrix repair processes.
Critical components that aided researchers in this discovery was the use of GE Healthcare’s CodeLink microarrays, which offered researchers higher sensitivity microarrays, and improved techniques for high-fidelity RNA amplification from small samples.
“The ability to identify even slight gene expression changes can have a huge impact on researcher’s understanding of the cellular processes involved in the onset and cascade of a disease,” said Chockalingam Palaniappan, Head of R&D in the Molecular Diagnostics division, GE Healthcare. “GE is pleased that its technologies, including the CodeLink UniSet Rat 10K Bioarray used in this study, are continually assisting researchers to make significant strides in preclinical research which will pave the way for better medical care in the future.”
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