Dr. Kernacki's studies were the first to show the protective features of TIMP expression against corneal detruction.

Corneal ulceration and tissue breakdown have been attributed to the destructive nature of MMPs, a family of proteolytic enzymes called matrix metalloproteinases. One way to stop corneal scarring and perforation, then, is to halt the action of the MMPs. What better way than to put their natural enemies to work?

Karen Kernacki, PhD, assistant professor of anatomy and cell biology, is fighting MMPs with their counterparts, TIMPs (tissue inhibitors of metalloproteinases). Previous studies have shown increased MMP expression in animals with ulcerative corneal disease. In a recent paper, published in Investigative Ophthalmology & Visual Science, Dr. Kernacki showed that inhibition of TIMP activity resulted in increased corneal tissue damage.

“Just as we suspected, TIMPs inhibited MMP activity, and controlled the cyclic destructive response, protecting the cornea from irreversible tissue destruction,” said Dr. Kernacki.

With more than $1 million from the National Institutes of Health, Dr. Kernacki is expanding her studies to investigate the behavior of MMPs and TIMPs in various models of corneal ulceration. She is testing different mechanisms and pathways to determine if the TIMPs exhibit protection similarly, regardless of the cause of injury. “Ulcers can be induced by bacteria, chemical injury or thermal injury,” Dr. Kernacki said. “We are trying to determine if the enzyme profiles are the same in each instance.”

Because corneal ulcers progress very quickly, a transplant may be the only treatment option available. If TIMPs can stop the damage in the first place, Dr. Kernacki hopes to reduce the need for corneal transplants and perhaps halt the ulceration completely.

Dr. Kernacki earned her PhD in immunology from Wayne State University. As a post-doctoral student, she studied inflammatory mechanisms in Dr. Linda Hazlett’s lab. She was appointed to the faculty earlier this year.