The Key To A Strong Heart Could Lie With Blood Vessels
The heart is made of muscle, and for it to function properly, that muscle has to be strong and durable. A condition called left ventricular non-compaction interferes with heart function and leaves the heart muscles weak and spongy.
A collaboration between Ashby Morrison, PhD, and NYSCF — Robertson Investigator Kristy Red-Horse, PhD, has uncovered a possible cause for left ventricular non-compaction: dysfunction in the formation of blood vessels. The researchers didn’t plan to study this condition when they began their work together, they were originally interested in the role of a certain molecule Morrison’s lab was looking at.
Morrison and Red-Horse are office neighbors at Stanford University, and when discussing their respective research, Morrison explained that she had been investigating the function of a molecule called Ino80 in yeast. Without it, yeast die. It is also found in a bunch of other organisms, but scientists don’t know much about its role in them.
Red-Horse was intrigued, and the two set out to investigate what happens when Ino80 is deleted from mice—either entirely or in a specific part of the body. What they found was that mice who had Ino80 deleted from their heart cells had improper formation of the blood vessels that typically feed heart muscle. And without the blood vessels to nurture them, the muscles ended up spongy and weak, just like in left ventricular non-compaction.
In a follow-up study, the researchers grew heart muscle cells and endothelial cells (the precursors to blood vessels) in a dish together. They found that when endothelial cells didn’t express Ino80, the heart muscle developed abnormally. This finding indicated that endothelial cells must produce a growth factor that stimulates cardiac muscle growth.
Future research will focus on identifying further characteristics of that growth factor and developing stem cell treatments for left ventricular non-compaction.