EAST LANSING, Mich. Scientists have long known that high blood sugar levels from diabetes damage blood vessels in the eye, but they didn't know why or how. Now a Michigan State University scientist has discovered the process that causes retinal cells to die, which could lead to new treatments that halt the damage.
Diabetic retinopathy is a common side effect of diabetes and the leading cause of blindness in young adults in the United States. It's estimated that between 40 percent and 45 percent of people diagnosed with diabetes have some degree of diabetic retinopathy.
Research by Susanne Mohr, MSU associate professor of physiology, found the siah-1 protein is produced by the body when blood sugar levels are high. She then discovered that the siah-1 protein serves as a type of chauffeur for another protein, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), shuttling the GAPDH into the nucleus of Mller cells, special cells that have contact with the blood vessels in the eye. When GAPDH accumulates in their nuclei, the Mller cells die, which leads to the vascular damage associated with diabetic retinopathy.
The research is published in the Jan. 29 issue of the Journal of Biological Chemistry.
"Our earlier research showed that high glucose levels cause GAPDH to accumulate in the nuclei of Mller cells in the retina," Mohr explained. "But we weren't sure how the GAPDH was getting in there. It doesn't contain any of the necessary signaling motifs. I read about the siah-1 protein and cell death in white blood cells in a Nature paper, so we decided to investigate them. We had no idea if the siah-1 protein was even in the retina."
Mohr's research also found that lowering levels of siah-1 proteins stopped GAPDH from moving into the nuclei of Mller cells, which stopped them from dying.
"This is very exciting," Mohr said. "We know that we can't regulate production of GAPDH because it's necessary for produ
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Michigan State University