Scientists at Mayo Clinic have shown for the first time that an adult stem cell variant circulating in adult human blood can be driven to form smooth muscle cells, which are key building blocks in blood vessel formation and also participate in coronary artery blockages.
The researchers used platelet-derived growth factor BB (PDGF-BB) to convert previously undiscovered circulating smooth muscle progenitor cells (SPCs) into smooth muscle outgrowth cells (SOCs). SPCs produced presumably reside in the bone marrow and are stem cells that have started down the path of cell differentiation. Scientists had suspected the existence of circulating SPCs because animal studies had shown that many smooth muscle cells found in atherosclerotic plaques or in restenosis after angioplasty had been partially derived from bone marrow.
The Mayo Clinic study is the first to prove the existence of SPCs in humans. In the presence of PGDF-BB, the cells rapidly proliferated into smooth muscle cells. These cells also had adhesive properties potentially steering the cells to areas of vessel blockages.
According to first author, David Simper, the study may be a significant step in the potential development of new vessels (angiogenesis) to provide blood circulation to diseased hearts. "Previous studies have shown that endothelial cells, which line blood vessels can be grown from progenitors in blood," says Dr. Simper. "Smooth muscle cells are the essential building blocks of arteries, and until now we have not had a way to create them".
These new findings may help cardiologists address in a new way some of the key problems in interventional cardiology. "About 30 percent of patients with heart disease who have stents implanted during angioplasty have problems with renarrowing, or restenosis, within the stents," says Noel Caplice, the director of the Mayo Clinic lab that conducted the study. "Smooth muscle cells are a major ingredient of these new blockages, which are the body's response to the injury of the artery wall during the angioplasty procedure. If the circulating blood is the source of cells that contributes to plaque formation, then perhaps therapy can be used to either prevent the progenitor cells from progressing to become smooth muscle cells, or eliminate the adhesive properties that cause them to home to the injury site. Furthermore, this study may enhance our efforts in achieving therapeutic angiogenesis."