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Injection reverses heart-attack damage
July 24, 2009Growth factor enhances heart regeneration, improves heart function without need for cardiac stem cells
Injured heart tissue normally can't regrow, but researchers at Children's Hospital Boston have now laid the groundwork for regenerating heart tissue after a heart attack, in patients with heart failure, or in children with congenital heart defects. In the July 24 issue of Cell, they show that a growth factor called neuregulin1 (NRG1), which is involved in the initial development of the heart and nervous system, can spur heart-muscle growth and recovery of cardiac function when injected systemically into animals after a heart attack.
After birth, heart-muscle cells (cardiomyocytes) normally withdraw from the cell cycle - meaning they stop dividing and proliferating. But the researchers, led by Bernhard Kühn, MD, and Kevin Bersell of the Department of Cardiology at Children's, were able to restart the cell cycle with NRG1, stimulating cardiomyocytes to divide and make copies of themselves -- even though they are not stem cells.
"Although many efforts have focused on stem-cell based strategies, our work suggests that stem cells aren't required and that stimulating differentiated cardiomyocytes to proliferate may be a viable alternative," says Kühn, the study's senior investigator and a practicing pediatric cardiologist at Children's since 2007.
When the team injected NRG1 into the peritoneal cavity of live mice after a heart attack, once daily for 12 weeks, heart regeneration was increased and pumping function (ejection fraction, assessed on echocardiograms) improved as compared with untreated controls. The NRG1-injected mice also lacked the left-ventricular dilation and cardiac hypertrophy that typify heart failure; both were seen in the controls.
When the researchers also stimulated production of a cellular receptor for NRG1, known as ErbB4, cardiomyocyte proliferation was further enhanced, demonstrating that NRG1 works by stimulating this receptor. They also identified the specific kinds of cardiomyocytes (mononucleated) that are most likely to respond to treatment.
In 2007, Kühn and colleagues first demonstrated that the heart has dormant regenerative capacities that can be reawakened. Kühn developed a sponge-like patch, soaked in a compound called periostin that is abundant in the developing fetal heart (and in injured skeletal muscle) but scarce in adult hearts. When the patch was placed over the site of cardiac injury in rats, it induced cardiomyocyte proliferation and improved heart function (Nature Medicine 2007; 13:962-9). Similar results were seen in larger animals, and periostin is now in preclinical development at Children's Hospital Boston for future application in human patients with heart failure.
The new work adds a second compound to the heart-regeneration toolbox, and reveals how both periostin and NRG-1 work at the cellular and molecular level, an essential step in predicting possible side effects. Both compounds ultimately act on the same cellular pathway, Kühn found.
"We applied periostin locally at the site of cardiac injury, but NRG1 works when given by systemic injection - a very promising result that suggests it may be feasible to use this in the clinic to treat heart failure," says Kühn, who won a first prize Young Investigator Award, from the American College of Cardiology in 2007.
Children's Hospital Boston
"Although many efforts have focused on stem-cell based strategies, our work suggests that stem cells aren't required and that stimulating differentiated cardiomyocytes to proliferate may be a viable alternative," says Kühn, the study's senior investigator and a practicing pediatric cardiologist at Children's since 2007.
When the team injected NRG1 into the peritoneal cavity of live mice after a heart attack, once daily for 12 weeks, heart regeneration was increased and pumping function (ejection fraction, assessed on echocardiograms) improved as compared with untreated controls. The NRG1-injected mice also lacked the left-ventricular dilation and cardiac hypertrophy that typify heart failure; both were seen in the controls.
When the researchers also stimulated production of a cellular receptor for NRG1, known as ErbB4, cardiomyocyte proliferation was further enhanced, demonstrating that NRG1 works by stimulating this receptor. They also identified the specific kinds of cardiomyocytes (mononucleated) that are most likely to respond to treatment.
In 2007, Kühn and colleagues first demonstrated that the heart has dormant regenerative capacities that can be reawakened. Kühn developed a sponge-like patch, soaked in a compound called periostin that is abundant in the developing fetal heart (and in injured skeletal muscle) but scarce in adult hearts. When the patch was placed over the site of cardiac injury in rats, it induced cardiomyocyte proliferation and improved heart function (Nature Medicine 2007; 13:962-9). Similar results were seen in larger animals, and periostin is now in preclinical development at Children's Hospital Boston for future application in human patients with heart failure.
The new work adds a second compound to the heart-regeneration toolbox, and reveals how both periostin and NRG-1 work at the cellular and molecular level, an essential step in predicting possible side effects. Both compounds ultimately act on the same cellular pathway, Kühn found.
"We applied periostin locally at the site of cardiac injury, but NRG1 works when given by systemic injection - a very promising result that suggests it may be feasible to use this in the clinic to treat heart failure," says Kühn, who won a first prize Young Investigator Award, from the American College of Cardiology in 2007.
Children's Hospital Boston
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Elevated biomarkers lead to diminished quality of life in heart attack patients post-discharge
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Tiny particles can deliver antioxidant enzyme to injured heart cells
Researchers at Emory University and the Georgia Institute of Technology have developed microscopic polymer beads that can deliver an antioxidant enzyme made naturally by the body into the heart.
New study links vitamin D deficiency to cardiovascular disease and death
While mothers have known that feeding their kids milk builds strong bones, a new study by researchers at the Heart Institute at Intermountain Medical Center in Salt Lake City suggests that Vitamin D contributes to a strong and healthy heart as well - and that inadequate levels of the vitamin may significantly increase a person's risk of stroke, heart disease, and death, even among people who've never had heart disease.
When seconds count: Interventional radiology treatment for pulmonary embolism saves lives
Catheter-directed therapy or catheter-directed thrombolysis-an interventional radiology treatment that uses targeted image-guided drug delivery with specially designed catheters to dissolve dangerous blood clots in the lungs-saves lives and should be considered a first-line treatment option for massive pulmonary embolism, note researchers in the November Journal of Vascular and Interventional Radiology.
Texas Children's discharges first pediatric patient with implanted mechanical heart device
Texas Children's Hospital is the nation's first pediatric hospital to discharge a child while on an intracorporeal ventricular assist device (VAD), a feat previously accomplished only at adult institutions.
Researchers develop innovative imaging system to study sudden cardiac arrest
A research team at Vanderbilt University has developed an innovative optical system to simultaneously image electrical activity and metabolic properties in the same region of a heart, to study the complex mechanisms that lead to sudden cardiac arrest.
Experts unveil new CVD guidelines and position papers
Several new guidelines and position papers offering the most up to date information to ensure that clinicians practice evidence-based medicine were released at the Canadian Cardiovascular Congress 2009 this week.
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