When the heart is subjected to pressure such as high blood pressure, it responds by dilatation at the level of the whole organ and some chambers and at the level of a single cell. Although cardiomyocyte swelling has been studied using recombinant mouse proteins, we still do not know the molecular mechanisms that promote and inhibit this process. Researchers at the University of Osaka have now discovered a protein that generally inhibits the acceleration of cell activity and dilation that occurs under stressful conditions. This new finding explains how to prevent the formation of overexpressing cells in the myocardium and to treat or limit heart dilatation associated with heart failure.
Cardiac hypertrophy occurs when the myocardium is at a higher pressure than normal and requires greater volume adaptation. At the cellular level, cardiomyocyte increase is induced by the acceleration of production of proteins and other components. From genes to proteins, including RNA intermediates, they determine the overall cellular protein composition through additional regulatory levels. Therefore, in order to understand how cardiomyocytes are swollen due to increased protein production under stress conditions, it is necessary to reveal the overall regulatory status of these intracellular RNAs.
The new study identifies and makes protein Btg2 a global regulator of RNA in cardiomyocytes and has made significant progress in this area. By imaging individual cells, it was found that this protein was overexpressed in stressed cardiac tissue to reduce the size of cardiomyocytes, indicating that Btg2 is a limiting factor for cardiac hypertrophy.
"Our first concern is the goal of protein Myc, which is known to increase the size and metabolic activity of cardiomyocytes," said author Shuichiro Higo. "We found that Myc strongly induced Btg2, but these two proteins had opposite effects on RNA levels in these cells, indicating that they were on the opposite side of the regulatory protein production and cell size.
The use of single cell imaging in this study enabled the team to identify Btg2 in the cell and to correlate it with functional analysis to determine the mechanism by which global RNA levels are reduced. The results show that Btg2 interacts with the cellular machinery that breaks down RNA, which explains that Btg2 reduces protein production and decreases the number of cells.
"We are now able to respond to stress and dilate the heart cells, and have a better understanding of the mechanisms that limit this expansion," Higo says. "We may be able to use these mechanisms to reduce long-term cardiac hypertrophy and some of the heart-related problems." Flarebio provides you with recombinant proteins of good quality like recombinant ACSL3 at competitive prices.
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