Featured Researcher
Nina Reiniger, PhD: Investigating Cellular Pathways of Diabetic Nephropathy
Nina Reiniger, PhD Nina Reiniger, PhD, Postdoctoral Research Scientist in the Division of Surgical Science, has always had a strong interest in the biomolecular foundations of human health.
"The human body is so intricate.
I've always thought it is amazing that it works as well as it does," she says.
Dr. Reiniger's scientific training and academic career have focused on the molecular disruptions of cellular systems and how they lead to various disease states.
A native of Vancouver, Canada, Dr. Reiniger earned her BS from Simon Fraser University in Burnaby, British Columbia in 1998 and then came to the U.S. to complete a PhD in microbiology and molecular genetics at Harvard University.
At Harvard, Dr. Reiniger studied the inflammatory process in the lung's response to bacteria.
Her research there, conducted under Dr. Gerald Pier, focused on cystic fibrosis, in which the congenital lack of a receptor in epithelial cells causes a destructive inflammatory response to bacterial infection, by Pseudomonas aeruginosa, in the lung.
Her journey to Columbia began when she changed her focus to diabetes, in which excess sugar in the blood stream causes destructive inflammatory responses throughout the body.
"I was interested in diabetes because it is a disease with an inflammatory component that does not involve infection," she says.
She began attending seminars at the Harvard-affiliated Joslin Diabetes Research Center.
She says that when she asked scientists at the Joslin for names of scientists investigating the area of diabetes and inflammation, the name Ann Marie Schmidt kept coming up.
Dr. Reiniger decided to approach Dr. Schmidt, who is Chief of the Division of Surgical Science in Columbia's Department of Surgery, for a diabetes-focused postdoctoral fellowship.
Contacting Dr. Schmidt and presenting her previous work, Dr. Reiniger received a positive response.
Together they designed a research plan to study a genetically engineered mouse model known as Db/Db that exhibits features of nephropathy (kidney disease) that are seen in diabetic humans. Later, this work was extended to include the OVE26 mouse model, which has more severe nephropathy that more closely resembles diabetic nephropathy in humans.
To support the research, they developed a NIH proposal, which was accepted for funding, and in January 2006, her PhD defense complete, Dr. Reiniger was accepted for a postdoctoral fellowship in the Division of Surgical Science.
Specifically, the research project, which entered its fourth year in January 2009, focuses on the contribution of the RAGE receptor molecule to diabetic nephropathy.
Its name a shortening of receptor for advanced glycation end-products, RAGE is present in many tissues throughout the body.
When activated, RAGE unleashes a series of destructive inflammatory processes contributing to a multitude of human disease states including atherosclerosis, cancer, and the many serious complications of diabetes.
To conduct the study, the investigators bred a genetically altered strain of OVE26 mice lacking the RAGE receptor.
Previous research in the Schmidt lab has included kidney studies of other diabetic mouse models, but none exhibiting nephropathy as severe as OVE26.
In addition, this was the first study where RAGE deletion and diabetes both had a genetic basis and did not rely on pharmacological agents.
The study's results, completed in the fall of 2008, showed that removing RAGE partially protected the new mouse strain against kidney disease.
"It was exciting to see how well protected it was from a very severe disease," says Dr. Reiniger.
Now, to analyze the biochemical specifics of the study's results, the team will spend two years performing microarray gene analysis on the mice.
Their goal is to find out which genes were turned on in the genetically altered OVE26 mice to launch the cell signaling changes that protected the animals' kidneys.
Dr. Reiniger says it is clear that removing RAGE from the picture has a beneficial effect, and that perhaps a drug inhibiting RAGE might produce the same effect in humans.
But she says disabling RAGE throughout the body might cause side effects because RAGE may have some constructive purpose in the body that should not be inhibited.
"It's naïve to think there's not some function of RAGE that's beneficial to us," she says.
The microarray analysis will be critical to developing a complete picture of the biochemical processes involving RAGE in the kidney disease cellular pathways.
"It would be ideal to target more specific interactions downstream of RAGE."
Dr. Reiniger, who lives with her husband on Manhattan's Upper West Side, has enjoyed her three years as a New Yorker and has kept busy with multiple interests.
In addition to cycling, piano, and photography, she competes in the ice-based rock-sliding sport known as curling, which has been a passion of hers since she was 13.
Dr. Reiniger and her three teammates will be competing in the Olympic curling trials for 2010 in February 2009.
As for the decisions she's made about the direction of her career, she's very satisfied.
"Diabetes is a wide-ranging disease that affects a large number of people and that is a strong motivation for me."
She says the Schmidt lab is a great lab to be working in.
"They gave me a lot of support for getting my project off the ground," she says.
"Ann Marie and her colleagues are wonderful scientists and always full of great ideas to keep the science rolling."
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