MONDAY, May 2, 2005 (HealthDay News) -- In research with mice, Japanese scientists found a way to use transforming growth factor (TGF)-beta to help the heart repair itself after a heart attack, according to reports in the current issue of Circulation.
TGF-beta, a protein that regulates immune response and plays a role in communication between cells, is released from cells in response to a number of stimuli, including stress. TGF-beta can have either a beneficial or harmful effect on heart cells.
In one study, researchers used TGF-beta to coax bone marrow stem cells into becoming heart cells. They treated the bone marrow stem cells with TGF-beta, and then injected the cells into the hearts of mice that had been induced to have heart attacks. After three months, the mice injected with the TGF-enriched stem cells showed improvement in blood flow to areas of the heart treated with the stem cells.
The treatment appeared to promote the growth of new blood vessels, and about 30 percent of the TGF-enriched stem cells had turned into heart muscle cells, the researchers said.
In the second study, scientists inhibited the function of TGF-beta to slow the damage the protein can cause following a heart attack. The researchers did this by injecting the mice with an artificial TGF-beta receptor on the third day after a heart attack. The artificial receptor inhibits the function of TGF-beta so it can't exert its negative effect.
Inhibiting TGF-beta directly protected cells in heart tissue damaged from blockages in the heart, the researchers found.
In a prepared statement, team leader Dr. Hisayoshi Fujiwara said many heart attack patients "miss the chance for coronary intervention because to be effective it must be performed within a few hours after the onset of heart attack. After this golden time has passed, there is no active therapy for patients at present. Our findings imply a new therapeutic strategy that is applicable even to the people who missed this golden opportunity."
"While no one knows how a protein can be both a bad guy and a good guy, the research suggests that timing is everything. Early on, TGF-beta seems to be a good thing, but after that window passes, it becomes deleterious and you want to block it," Ronglih Liao, co-director of the Cardiac Muscle Research Laboratory at the Whitaker Cardiovascular Institute in Boston, wrote in an accompanying editorial.
"Within the first 24 to 72 hours following cardiac injury, locally released TGF-beta 1 may promote regeneration, but after this stage it may be detrimental," Liao noted.
The Cleveland Clinic Foundation has more about heart attacks.