Department of Physiology associate professor Susanne Mohr poses with a dissecting microscope in her lab in the Biomedical and Physical Sciences Building. Mohr did research using mouse retinas to determine which retina cells were damaged from diabetes.
Research completed by a team of scientists, including an MSU professor, might lead to a new type of treatment in curing diabetic blindness.
Susanne Mohr, an associate physiology professor at MSU, spent more than two years working with E. Chepchumba Yego, a former graduate student at Case Western Reserve University in Cleveland, to find a way to treat retinopathy. The team’s research appeared in the Jan. 29 issue of the Journal of Biological Chemistry.
In retinopathy, Mohr said the cells surrounding the vascular die and leave the vascular unprotected with no support from the surrounding cells. Once the protecting cells are gone, different fluids from the brain leak into the retina, causing bruising.
Current treatment for retinopathy can be uncomfortable to patients because it involves eye shots or laser treatment, Mohr said.
“A retina can only be lasered two or three times before blindness from lasering happens,” Mohr said. “That’s it. We have no other treatment. The field is desperate for anything that can help that can be put into a treatment.”
Before Mohr began her research, it was unknown how the cells died. Mohr said the team found a way in which cell death is induced in a high glucose environment. The enzyme glyceraldehyde 3-phosphate dehydrogenase, or GAPDH, moves from its cytosolic environment to the cell’s nucleus to create energy, where cell death occurs.
“You’re never really convinced that it would work,” Mohr said of her team’s discovery. “When we did the first siah-1 (protein) experiment it was pretty exciting. It’s really cool when something really works. Yes, we do celebrate these experiments.”
The team’s discovery of the siah-1 protein was the breakthrough for Mohr. The siah-1 protein can be manipulated to keep any cell death from occurring and therefore reducing the effects of retinopathy, Mohr said.
“The question is how does (GAPDH) get from one cell part to the other location,” Mohr said. “We found that the siah-1 protein is the carrier of GAPDH to that location.”
About 5 million people have diabetic retinopathy, according to the World Health Organization. It is estimated that 80 percent of Type 2 diabetic patients progress into some stages of diabetic retinopathy, Mohr said. Type 2 diabetes patients are growing exponentially, which causes a much larger number with the disease, she said. Retinopathy develops five to 10 years after a person is diagnosed with Type 2 diabetes, Mohr said.
“(There are) Type 2 diabetic patients with heart disease that are 16-year-olds,” Mohr said. “They are going blind in their 20s.”
Because people are developing diabetes at younger ages, the concern for a better treatment is pressing, Mohr said.
Yego said it was great to complete the project and contribute new research.
“It was exciting to create a new thinking in the field,” Yego said. “It was like something that is new. No one has thought of (this) before.”
William Spielman, chairman of MSU’s Department of Physiology, said Mohr’s research is important because it explains the vascular damage that has been caused by diabetes.
“The biggest reason we recruited her was because of her research,” Spielman said.
Mohr said she will continue research on the project at MSU with Yego. Mohr said continuing the research involves understanding what happens in the nucleus regarding the death of cells and animal testing.
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