Cardiovascular disease is one of the health conditions that many people suffer and die from around the world — it is common to have someone very close to you fall victim to it. As ubiquitous as cardiovascular disease is, so are the efforts to treat it.
Dave Vereide, the Morgridge Fellow of the Thomson lab, pioneers the expansion of vascular disease knowledge with a hallmark stem cell model for a better cure. He specializes in arterial stem cell research.
Vereide studies a new method to create human arterial endothelial cells from cord blood and adult bone marrow sources, which are extremely difficult to procure in large quantities but essential in engineering efforts to combat heart disease.
One of the major risk factors for the congenital heart disease is the transition of endothelial cells to mesenchymal cells. In essence, it is a shift from a cell that retains healthy arterial properties to a compromised cell that hardens the arteries. The transition from endothelial to mesenchymal cells is linked to major cardiovascular conditions such as arteriosclerosis.
Vereide comments that such a transition is “a naturally occurring transition that’s probably healthy, like in a response to injury.” However, he adds that cardiovascular diseases shift this balance by allowing too many transitions to take place, resulting in massive deleterious effects.
What Vereide aims to achieve from his model is to gain a better understanding of this occurrence and to use that knowledge to procure more viable treatment options for heart conditions.
Vereide described his method as a comparative model between endothelial cells and mesenchymal cells. He assembles the cells in two forms in a dish; one form is resistant to the mesenchymal transition and the other form is susceptible to such a shift. He said that this environment mimics the mischievous mesenchymal transition of endothelial cells.
This model offers researchers a better understanding of the cells’ biology, which will allow them to develop more specific drugs or refined therapy options from the direct insertion of transcription cells from bone marrows that could cause proliferation that target the damaged parts.
He suggested that this method may not only be used to study the causes and cures of artery hardening, but could also be expanded to other health failures found in kidneys, lungs or even the opposite cell transition: the weakening of the arteries that could result in strokes.
With this research, Vereide expressed that researchers could potentially use this strategy to develop artificial arteries or organs to surgically implant in patients, as well as other ways to use cells without disrupting the body of the patient. However, such advances will not occur for a stretch of years.
In the short term, he hopes that this technique will be valuable in cellular therapies and drug development. Since many possible research paths have opened up, Vereide impressed that it is hard to predict where the research will exactly go in terms of directions and outcomes.
In the future, researchers could make discoveries that may not be imaginable today, but would contribute to the constantly changing purpose of the scientific study.
