Researchers say, bone marrow nerve damage has been found to play a crucial role in blindness-causing complications in diabetics.
According to Julia Busik, an associate professor in MSU's Department of Physiology, the key to better treating retinopathy damage to blood vessels in the retina that affects up to 80 percent of diabetic patients - lies not in the retina but in damage to the nerves found in bone marrow that leads to the abnormal release of stem cells.
"With retinopathy, blood vessels grow abnormally in the retina, distort vision and eventually can cause blindness," said Busik.
"There has been a lot of progress in treating the complication, but most treatments use a laser that is painful to the patient and destroys parts of the retina," she added.
The research team found that nerve damage in diabetic bone marrow - where stem cells known as endothelial progenitor cells reside - affects the daily release of those EPCs into the bloodstream.
Normally EPCs would exit the bone marrow and repair damage done in the vascular system during sleep.
Using animal models, the research team observed that the pattern of EPC release is faulty in diabetic bone marrow, creating abnormally low levels of EPCs during sleep, when they are needed most.
That decrease in EPC release from a diabetic patient's bone marrow preceded the development of retinopathy.
"When the bone marrow suffers nerve damage in diabetic patients, it no longer provides a signal for the timely release of these reparative stem cells," Busik said.
This novel finding shows that bone marrow nerve damage represents a new therapeutic target for treatment of all diabetic vascular complications, such as retinopathy.
"This opens up new avenues to better treatments outside of the retina that focus on stem cells and the causes of the nerve damage in bone marrow," said Busik.
"We know what happens in the retina and have treatments that are very invasive; we now can look at a host of other options," she added.
The research appears in the Journal of Experimental Medicine.