UC Berkeley scientists published a report this week in the journal Nature Communications saying that they have isolated a type of stem cell that causes heart disease in later life.
The research is profound because it contradicts much of the generally accepted theories of what causes arterial hardening, and the concept may also relate to many other diseases could the associated stem cells be pinpointed.
What senior author Song Li, a bioengineering professor at UC Berkeley and a researcher at the Berkeley Stem Cell Center, and his team have uncovered is a dormant stem cell in blood vessel walls, that seems to sit inactive for most of a person’s lifetime, before coming to life and causing less functional cells to begin to grow. Li says these new types of cells that start growing in later life, are the root cause of arterial hardening and clogging that are associated with deadly strokes and heart attacks.
Originally, it was thought that the smooth muscle cells in the arteries lining become scarred over time, and this leads to the narrow and brittle arteries that play a major part in causing cardiovascular disease. Not so says Liu: Essentially, what the scientists are saying is that the smooth muscle cells are not to blame. Rather a different kind of stem cell, that Li calls multipotent vascular stem cells, kicks in, and begins growing cells that look much like the smooth muscle cells, but don’t function correctly. The cells were not found previously, because there are so few of them, that they were hard to isolate.
“We call them sleeping beauty or sleeping evil cells, because they don’t do anything when they’re dormant. The stem cells stay quiescent for decades before they start to grow and they make the blood vessels harden.”
It almost sounds like something from Blade Runner, where the replicant humans have been deliberately designed to deteriorate and die at a much faster rate than the natural ones. What purpose would it serve the body under standard evolutionary terms to have cells activating later in life that effectively lead to its demise? With the arteries poorly formed, with wrong cell types, the blood flow becomes slowed and can then stopped completely. This causes strokes or heart attacks, depending on the location of the blockage. Strokes and heart attacks are one of the leading causes of death in the United States.
Creating drugs or other genetic treatments to shut down these stem cells or even deactivate them while a person is still young has the potential in the future to prevent arteriole hardening, reverse the damage already done, and even make this type of cardiovascular disease a thing of the past. Perhaps the futuristic Woody Allen movie “Sleeper” where people smoke tobacco and eat a high fat diet because it’s healthier is not so far fetched after all.
Li backs up his theory by pointing out that the current ideas, of smooth muscle cells in the artery walls, “dedifferentiating”, or basically reverting back to an earlier stage of development and causing the scaring and degeneration seen in hardened arteries, actually had no fundamental proven mechanism to back it.
Li traced the lineage of the cells back to the multipotent vascular stem cells, which are able to form several types of cell, including the smooth muscle cells.
Dr. Deepak Srivastava, director of the Gladstone Institute of Cardiovascular Disease at UCSF, who provided mouse tissue samples to the UC Berkeley scientists but was not involved in the research commented on the dramatic findings:
These findings shift the paradigm … If the new data holds up, the target for treating vascular disease may be very different than what we’ve been aiming at … Maybe the reason we’ve met with limited success in treating heart disease is because we’ve been going after the wrong target.”
It is worth noting, of course, that the research is ground breaking and will need to be repeated and confirmed by other research teams, and Li did most of his work on mouse rather than human tissue. Nonetheless, it is an impressive work and one that will soon give drug companies a target to begin preventing growth of these negative “death” cells.
Interestingly, the stem cells that form arteries are also capable of becoming nerve, cartilage, bone and fat cells, suggesting why arteries become brittle or even filled with fat deposits. Li says that trying to attack the problem with diets and lower cholesterol is just attacking the symptoms, much like trying to stop a runny nose when you have a cold.
The research is certainly eye opening, and when we think back 100 years to some of the more outlandish scientific theories that have long since been discarded, it doesn’t require much stretch of the imagination to realize that there must still be theories taken to be practically a fact, that are at best misleading or at worse plain wrong. In the spirit of a true scientist, Li has reminded us that we have so much more to understand about our existence.
Written by Rupert Shepherd