For the last 15 years, researchers had known that there is a movement of a specific type of cells present in the bone marrow, known as the progenitor cells, to the heart after it suffers from an attack. Similarly, researchers knew that the movement of microRNAs increases after a heart attack. Despite this information, there wasn’t much progress in the research of immediate heart muscles’ repair after an attack.
However, there has been a breakthrough in research led by Gangjian Qin, M.D., the director of the Molecular Cardiology Program and a professor at the University of Alabama’s Department of Biomedical Engineering, and Min Cheng, M.D., Ph.D., Huazhong University of Science and Technology, Wuhan, China, published in “Nature Communications”. It found that exosomes, which are extracellular vesicles released from cells, play an essential role in conveying information from the heart muscles in case of an attack. They communicate this information via cells by maneuvering through proteins, and other compounds present within them.
The observations on both, mice and humans, have shown that these exosomes carry large amounts of microRNAs, specific to the heart after it suffers from an attack. They are carried to the cells present in the bone marrow, where they shut down a particular gene. As a result, the bone marrow releases the progenitor cells, which flow through the bloodstream, reach the heart, and try to repair the damage.
This repair mechanism is being considered a breakthrough in the domain of research specific to heart repair after an attack.
Details of Research
In both, humans and mice, there are four types of microRNAs which are specific to the heart muscles, also known as the myo-miRs or miRNAs. These four types include, mirR-1a, miR-133a, miR-208a and miR-499-5p. They are tiny, non-coding RNAs, which can regulate the translation of information held within a gene into RNA structures. The set of genes present in a single human cell produce at least 2,000 varying miRNAs.
Observations on the mouse model showed that the levels of myo-miRs are escalated around 10,000 to 100,000 times in the bloodstream whenever there is a heart attack. They replaced a large quantity of the mononuclear cells present in the bone marrow and a few present in the kidneys. However, among the four types, miR-1a, miR-208a, and miR-499-5p traveled to the bone marrow in larger quantities; whereas, the fourth one’s amount was much lesser. This mechanism was also found in humans’ bodies after they suffer from a serious type of cardiac arrest in which heart’s major arteries are blocked, medically termed as STEMI (ST-elevation myocardial infarction).
Researchers knew that a chemokine receptor termed as CXCR4 is blocked after a heart attack, which facilitates the movement of progenitor cells present within the bone marrow through the bloodstream to attempt repairs of heart muscles. Thus, it was deduced that the damaged heart prompts the bone marrow progenitor cells to mobilize.
Researchers are confident that the heart muscles’ tissue repair procedure after a severe heart attack, discovered in this study, might prove to be a breakthrough in the domain of Cardiac Ischemia.
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