The study identifying the RNA-binding protein SRSF3 as an essential factor; for proper heart contraction and survival. But finding that the loss of cardiac expression of SRSF3 leading to a critical reduction; in the expression of genes involve in contraction.
Study of the mechanism of action of SRSF3 in the heart could open the way to the design of new therapeutic approaches for the treatment of heart disease. As the cardiovascular disease is the leading cause of death in the world. In 2015 alone; cardiovascular disease killing 17.7 million people; with 6.7 million of these deaths caused by heart attack. Unfortunately, knowledge is limited about the molecular mechanisms that regulate progression of a myocardial infarction; hindering the development of new therapeutic approaches.
Proper heart contraction
The recent development of massive-scale messenger RNA (mRNA) sequencing technology has permitted the identification of gene expression patterns associated with the development of heart disease. RNA-binding proteins perform important tasks in the cell.
However, by understanding of posttranscriptional regulation (a type of gene regulation) remains limited, in particular about the roles played by RNA-binding proteins (RBP) in myocardial infarction and the development of heart disease. But in this study investigating the role of the RBP SRSF3 in the heart, which was unknown until now. Finding that during embryonic development SRFS3; is expressing at high levels in cardiomyocytes and regulating their division.
But developing a genetically modifying mouse model that allowing them to eliminate SRSF3 expression specifically in cardiomyocytes; at a specifically scheduled time. The scientists found that elimination of SRSF3 from adult myocytes had a dramatic effect, severely impairing heart contraction.
But the mechanism through which SRSF3 supports heart contraction, the team compared the expression pattern and alternative processing (splicing) of all the mRNAs expressing in the hearts of mice lacking SRSF3 with results from control mice. Study finding reducing expression levels of mRNAs encoding protein components of the sarcomere, the physical contractile apparatus within cardiomyocytes; This reduction in the absence of SRSF3 was due to the degradation of these mRNAs, caused by the loss of a chemical modification, called the cap, at the 5′ end of mRNAs that, among other functions, protects them against degradation.