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A study at the University of Michigan's Health System laboratory has revealed a key trigger for producing normal red blood cells, which may pave the way for new and more effective treatments for patients with sickle cell disease.
In a project that marks the first time specific proteins have been targeted to prevent a disease, scientists increased the expression of proteins TR2 and TR4 to more than double the level of foetal haemoglobin produced in sickle cell mice, reducing organ damage.
"The vast majority of sickle cell disease patients are diagnosed early in childhood when adult haemoglobin normally replaces foetal haemoglobin, but the severity of the disease can differ markedly, correlating most strongly with the level of foetal haemoglobin present in red cells," said Dr Andrew D Campbell, lead author of the study.
It is hoped that the concept of the study, which included contributions from paediatric haematologists, cell and developmental biologists and pathology experts, could be applied to humans in future following clinical trials.
"Currently hydroxyurea is the only FDA approved drug known to increase the levels of foetal haemoglobin within sickle cell disease patients and a substantial number of patients do respond to it," added Mr Campbell.
"But the long term consequences for hydroxyurea are unknown, especially in children."
Sickle cell disease, or sickle cell anaemia, causes lifelong debilitating pain episodes, chronic organ damage and a severely shortened life span in sufferers.
In a study reported last month, researchers at Harvard Medical School identified that the disease may be reversed by turning off a single gene in red blood cells that causes the sickle cells to be produced.
Turning off the gene BCL11A, one of the molecular "switches" that stops production of foetal haemoglobin soon after birth, was found to alleviate the symptoms of sickle cell disease in mice, although researchers warned the treatment may be much more complex when applied to humans.
Posted by Alex Franklin Stortford
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