Cardiovascular disease is the leading cause of death worldwide. The regenerative biology team at Morgridge Institute unexpectedly discovered a powerful new model that can be used for studying vascular disease markers while studying laboratory arterial endothelial cell growth. The final result is published in the Journal of Stem Cell Reports, by Dave Vereide, a researcher at the Morgridge Institute.
In the report, a new method for producing human endothelial cells from cord blood and adult bone marrow sources is introduced. These cells, which are known to be difficult to grow stably, are crucial for the future role of tissue engineering against heart disease. But the second feature of these cells may be more influential. Vereide, one of the researchers in Morgridge Institute, claiming that these cells can perform two different states: one that maintains their healthy arterial properties over multiple generations of growth, and the second quickly turns identity into a type of damaged cell that is closely related to atherosclerosis or atherosclerosis. This change in identity, known as the transition of endothelial cells to stromal cells, is widely recognized as a major risk factor for congenital heart disease, vital organ fibrosis, hypertension and heart attack.
Vereide said the structural changes of both cell types are quite obvious. Endothelial cells have an elongated shape and tend to grow in a smooth, unicellular layer containing the arterial inner surface. In contrast, mesenchymal cells become more star-shaped and can deposit calcified extracellular matrix that tends to accumulate in arteries. Vereide says interstitial cells can also pack together, leading to thickened or bursting arteries that contract blood flow.
Assembling these new cell lines in a single dish, both forms - one that resists mesenchymal transition and one that is clearly sensitive to it - is not only essential for understanding this change, but also for developing inhibitory drugs.
While creating new cell lines, the research team used two transcription factors - or proteins that control specific genetic functions - which are known to be important for a wide range of cell types. But it turns out that they almost completely regulate the growth of arterial endothelial cells along with binding.
Vereide regarded it as a "super-lucky" coincidence. For the vast majority of possible problems in the circulatory system, almost all are related to arterial dysfunction which makes the arterial endothelium the main target of discovery. Until recently, scientists were still unable to grow these cells in vitro, and these arterial cells from the corpse will quickly lose arterial traits and do not proliferate for a long time. Vereide also claimed that now they have a line of research focused on cell therapy, and the other focused on drug development.
The next challenge is to find the genetic differences between these cells. Researchers will admit to finding targets for drugs or small molecules that can suppress the shift in the disease. Just as a large class of statins has revolutionized hypercholesterolemia, there may be a new class of drugs that can attack this major precursor of atherosclerosis, which can also be used for cell therapy.