Vascular development is an important process of embryonic development, and studying the molecular mechanism of vascular development has important physiological and pathological significance. MicroRNA-126 is a microRNA (miRNA) specifically expressed by endothelial cells, which is involved in regulating angiogenesis and maintaining vascular integrity, but its specific mechanism of action remains to be further elucidated.
The research team of Jingqing Jing and the research team of Liu Tingli used zebrafish as a model organism and found that there are two miR-126 sites (miR-126a / b) in the zebrafish genome, which can produce maturation in vitro and in vivo Biologically active miRNA. The research results were published in the journal Circulation Research.
The study found that miR-126a / b is involved in regulating embryonic vascular integrity and has a synergistic effect. Further research shows that miR-126a / b can regulate the integrity of blood vessels by regulating the expression level of pak1 in endothelial cells. This study broadens the understanding of the miRNA function of endothelial cells, helps to elucidate the mechanism of miRNA regulating vascular development and explore the pathogenesis of structural vascular diseases.
In June this year, the research team of Jing Qing researchers also deeply studied the role of microRNA-1 (miR-1) in cardiac hypertrophy and its regulatory mechanism, and found that miR-1 is the most abundant miRNA in the heart and is specifically expressed Cardiomyocytes. The research results were published in the international academic journal Journal of Cell Science.
Myocardial hypertrophy is the hypertrophic growth of the heart under various physiological stimuli, tissue damage or endocrine disorders. Myocardial hypertrophy is an initial adaptive response in function, which helps to increase the contractility of the heart and maintain the blood output of the heart, but continuous hypertrophy will eventually lead to heart failure and sudden death. Therefore, research on the pathogenesis of myocardial hypertrophy has been a hot issue in life science research. Recent studies have shown that a new gene regulator, microRNA (miRNA), is involved in the development of cardiac hypertrophy. However, the research on the role and mechanism of miRNA in the process of cardiac hypertrophy is still in its infancy and needs to be further elucidated.
In this article, the researchers delved into the role of microRNA-1 (miR-1) in cardiac hypertrophy and its regulatory mechanism. The study found that miR-1 is the most abundant miRNA expressed in the heart and is specifically expressed in cardiomyocytes. Further research found that the expression level of miR-1 was down-regulated during myocardial hypertrophy, and proved that miR-1 has the effect of inhibiting cardiomyocyte hypertrophy. Importantly, the study further confirmed that twinfilin-1, a cytoskeletal binding protein, is a target gene of miR-1, and reported for the first time that this protein has a role in promoting cardiomyocyte hypertrophy.
These results indicate that after the heart is hypertrophic, the reduction of miR-1 level causes the expression of twinfilin-1 to be up-regulated, which leads to myocardial hypertrophy by regulating the myocardial cytoskeleton. This research not only broadens the understanding of the molecular mechanism of myocardial hypertrophy, but also helps to elucidate the molecular mechanism of miRNA regulating myocardial hypertrophy, and provides a new theoretical basis and potential targets for the treatment of myocardial diseases. value. Related research has applied for a patent.
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