“Latest Stem Cells News”

Dean Third used to look forward to weekends spent refereeing local football matches, and outings with his young family. But now even walking to the end of the road can leave him breathless and exhausted.

For the past four years, the father of four has suffered from dilated cardiomyopathy (DCM), a disease of the heart muscle which causes it to enlarge, affecting its ability to pump blood to the arteries.
The condition afflicts 12,000 people in the UK, and for most sufferers the cause is unknown. If uncontrolled it can be fatal, and patients must adhere strictly to a regime of medication.

For Dean, a mature student from Brightlingsea, Essex, the only chance of a normal life is a heart transplant. But he says: ‘I am way down the list because there are so few. I may die before one becomes available.’
Dean, 39, also has to live with the knowledge that he may have given the disease to his children. Although his wife, Cathy, 40, does not have it, there is a 50 per cent chance he could have given it to Nadine, 16, William, 14, Ross, 12, and Charlotte Rose, nine.

They will have to be monitored for the rest of their lives.
However, Dean has just taken part in a BBC Horizon TV programme where he discovered that medics are on the brink of a major breakthrough, meaning conditions such as his could be cured by making new hearts from the patient’s own stem cells.

Often referred to as the body’s ‘building blocks’, stem cells have the remarkable potential to develop into many different cell types in the body during early life and growth. In addition, in many tissues they serve as a sort of internal repair system, dividing without limit to replenish other cells as they die out.

When a stem cell divides, each new cell has the ability either to remain a stem cell or become another type of cell with a more specialised function, such as a brain cell, a red blood cell or, as Dean learnt, healthy heart cells.
The documentary team examined the cases of three patients with chronic conditions to discover whether, within their lifetimes, they might be cured.

Dean visited Dr Anthony Mathur, from University College London, to witness the world’s first trial using stem cells taken from bone marrow. The cells are injected into the muscles of the heart to regenerate damaged tissue.
He also travelled to Minnesota in America to visit laboratories carrying out research to produce new hearts using stem cells (…)

But the prospect of creating new functioning hearts from a patient’s own tissue is now a real possibility. While researchers have yet to get results in human subjects, scientists at the University of Minnesota have produced new working hearts using rats’ and pigs’ stem cells.

Dr Doris Taylor, of the Centre for Cardiovascular Repair, has taken a heart from a dead rat and drained it of all its stem cells so that it is nothing more than a lump of protein, a process called whole-organ decellularisation.
She then took stem cells from a live rat and injected them into the inert heart. The stem cells are able to recognise it is a heart and begin working to form new cells, producing a new organ (…)

Read more: http://www.dailymail.co.uk/health/article-1222671/Well-soon-building-new-hearts-order-just-24-hours-say-stem-cell-scientists.html

It has long been thought that damage to the heart is irreversible, but new research is challenging that assumption.
Investigators from Children’s Hospital Boston were able to reverse heart damage in mice by stimulating the growth of new heart muscle cells.

They did this by injecting the mice with the growth factor neuregulin1, which is a key player in heart cell growth.
Until recently, most experts believed that the heart muscle could not repair itself, in part because the cells responsible for its development stop proliferating after birth.

But recent studies have shown that these heart muscle cells, known as cardiomyocytes, do have a limited ability to replace themselves.
The hope is that neuroregulin1 can one day be used to ramp up this process in humans and help heal damaged hearts, as it seems to do in mice, study co-author Bernhard Kuhn, MD, tells WebMD.

“Contemporary heart failure treatment is directed at making the remaining cardiomyocytes function better, and improvements in outcomes are harder and harder to achieve because these therapies have become so good,” he says. “But despite this, heart failure is still a fatal disease. Therapies that replace lost heart muscle cells have the potential to greatly advance the field.”
Injections Reversed Heart Attack Damage

Many other research teams are looking for ways to repair damaged heart muscle, but most of these efforts have focused on coaxing stem cells to become new heart cells.

The research by Kuhn and colleagues shows that stimulating heart muscle cells to proliferate in other ways may prove to be a viable alternative to stem cells, Duke cardiologist Richard C. Becker, MD, tells WebMD.
Becker, who is a spokesman for the American Heart Association, called the new research compelling.

“This is something that I suspect people in the field of cardiology will be very excited about, and I suspect this interest will stimulate additional research,” he says.
The mice in the study were treated with daily injections of neuregulin1 starting a week after experiencing laboratory-induced heart attacks.

Twelve weeks later, they showed evidence of better heart function, reductions in heart muscle scar size, and an increase in heart muscle cells, Kuhn says.
And unlike untreated controls, the treated mice showed no evidence of heart failure.

“Most of the [heart attack] related cell death had already occurred,” he says. “When we began the injections we saw replacement of a significant number of cardiomyocytes resulting in significant structural and functional improvements in the heart muscle.”
Researchers Studying Other Compounds
Neuregulin1 is not the first substance identified by the authors that promotes heart muscle cell growth.

In 2007, they reported that the protein periostin, found in the developing fetal heart and injured skeletal muscles, also induced cardiomyocyte production and improved heart function in rats.
Periostin cannot be injected, so the researchers developed patches infused with the compound, which were placed directly on the damaged area of the heart.

Kuhn says the two therapies may one day prove useful in the treatment of heart attack patients.
“During initial treatment patients might receive neuregulin injections, and once they are stable and out of the ICU they might be taken to the cath lab for a periostin patch,” Kuhn says.

But before that happens, the two treatments must be proven safe and effective in large animal and human studies.
The researchers recently completed a study of periostin in pigs, but the findings have not been published.

from webMD

In the near future, hearts that have just suffered a heart attack will be able to repair themselves, according to an incredible discovery of how to reeducate cardiac stem cells to repair damaged hearts. In fact, stem cells normally perform the delicate task of repairing cardiac muscle, but after a heart attack the cells no longer carry out this highly important self-repair.

Italian scholars at the ‘Sapienza’ University in Rome and the European Molecular Biology Laboratory (EMBL) in Monterotondo, have discovered why these cells stop functioning correctly, and now understand how to induce them to repair damage from heart attacks. The announcement was made during the 69th Congress of the Italian Society of Cardiologists in Rome by Professor Antonio Musaro’ of the ‘Sapienza’ University in Rome.

Musaro’ said, “With our studies conducted together with Doctor Nadia Rosenthal of the EMBL we have learned why stem cells present in the heart after damage from a heart attack or trauma, do not correctly function. In fact, instead of producing functional contractile tissue that allows the damage to be ‘repaired’, they stop functioning or even produce non-functional fibrous tissue. This occurs because the heart attack or damage creates an environment that is hostile to normal stem cells activity.”