The leading cause of death worldwide is not smoking, car crashes, or diabetes. It’s atherosclerosis.
Atherosclerosis is a disease in which plaque builds up in the arteries, making it difficult for oxygen-rich blood to reach the heart. Once the plaque ruptures, a clot forms and blocks the blood flow to a patient’s heart and causes heart attacks or strokes. In order to fight this disease, it is important to identify the source of the plaque ruptures.
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In the past, researchers believed that smooth muscle cells formed walls to prevent fats from accumulating as plaque. Thus, people believed that the more smooth muscle cells in the arteries, the better.
However, researchers at the University of Virginia School of Medicine may challenge the current treatment plan for patients. They discovered that they failed to identify 82% of the smooth muscle cells with the immunostaining methods used to detect atherosclerotic cells. Updated research has shown that some of the smooth muscle cells are actually building onto the plaque. The new questions become, ”What are these cells doing?” and “Why are these cells here?”
Some smooth muscle cells have been found to form the walls to prevent fats from accumulating, but some contribute to the plaque formation. This complicates things because scientists are confused about whether or not to encourage the growth of smooth muscle cells since they are both helpful and unhelpful.
To further add to the problem, some smooth muscle cells were being wrongfully identified as macrophages, while some macrophages were being misidentified as smooth muscle cells. Macrophages are cells in the immune system that target and destroy damaged or dead cells. This makes it more difficult to differentiate between the smooth muscle cells that have differentiated into macrophages and the smooth muscle cells that are beneficial to the system.
To begin the progression toward further study, Ph.D. student Laura S. Shankman has begun a technique for tagging the smooth muscle cells in their early growth stages. This allows for researchers to study how the smooth muscle cells develop when the plaque ruptures.
In her study, Shankman used male mice and split them into groups based on their genotype for various randomized experiments. Then, Shankman activated the Cre recombinase enzyme in order to effectively knock out the Klf4 gene. This way, she could determine whether the gene was responsible for the transformation of the smooth muscle cells.
In the end, Shankman discovered that gene Klf4 is responsible for the transformation of the smooth muscle cells. When the Klf4 gene was removed, the smooth muscle cells actually changed their functional properties to become more beneficial in curing the disease. In this way, the researcher realized that the Klf4 gene can help turn the “bad cells” into “good cells.” This marks the beginning of the long journey of curing the leading cause of death worldwide.
Featured Image Source: globe by Neil Tackaberry
