April 22, 2004
Heart tissue regeneration not working with stem cells, Murry finds
Researchers at the UW School of Medicine have found that bone marrow stem cells do not convert into heart muscle cells in mice. These results contradict a study conducted elsewhere that had prompted human clinical trials for such stem cell therapy in the treatment of heart attack.
Dr. Charles Murry, associate professor of pathology, led a team of researchers at the UW and the Wells Center for Pediatric Research at Indiana University during a two-year study of stem cell therapy. They injected haematopoietic stem cells (HSCs), which typically form blood cells, into the wall of the heart in both normal mice and in mice with hearts damaged by heart attacks.
Murry and his colleagues found that the stem cells did not convert into heart muscle cells in either group, and the damaged heart muscle tissue did not regenerate. The results represent a break from previous research, including a study published three years ago [“Bone marrow cells regenerate infarcted myocardium,” Orlic et al., Nature 410, 701 – 705 (2001)] that indicated such stem cells could help regenerate damaged heart muscle tissue after a myocardial infarction.
Murry’s results will be published in an upcoming issue of the journal Nature, and were published online March 21. A study at Stanford University showing results similar to those in Murry’s paper will appear in the same issue. Because both studies show that the stem cells do not convert as expected, these findings call into question the results from the Orlic study published in 2001.
“That group’s work is simply not reproducible,” said Murry. “Their study prompted a series of premature clinical trials for the treatment of acute heart attacks, which are still going on now.”
Despite the absence of muscle regeneration, Murry thinks there could be potential benefits from stem cell therapy in damaged hearts. The cells could help increase blood flow in the vessels surrounding damaged cardiac tissue, or the cells could help prevent “remodeling” in the heart, which is when the heart expands after a heart attack. That dilation can damage the heart muscle, Murry said, so preventing the dilation could help avoid the damage.
“Now that the trials are under way and appear safe, it is probably worthwhile continuing to see whether they are effective,” Murry added.