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Sep 18, 2009

Einstein Obtains $3.5M to Study Epigenomics of Abnormal Fetal Growth and Chronic Kidney Disease

  • NIH awarded Albert Einstein College of Medicine of Yeshiva University two grants totaling $3.5 million to study epigenetic modifications. Specifically, they will look at how these chemical modifications of genes relate to abnormal fetal growth and chronic kidney disease.

    The money is part of 22 grants totaling $62 million that the NIH is doling out over the next five years to bolster epigenetic studies. “Epigenomics represents the next phase in our understanding of genetic regulation of health and disease,” says NIH director, Francis Collins, M.D., Ph.D. “These awards will address the extent to which diet and environmental exposures produce long-lasting effects through changes in DNA regulation.”

    Einstein’s projects will focus on DNA methylation, often associated with silencing of nearby genes. The larger of the two grants awarded to Einstein for $2.03 million over five years will address the epigenetic changes that influence abnormal fetal growth.

    “We know that very small and very large newborns have a higher chance of developing problems like diabetes or cardiovascular disease later in life,” says Francine H. Einstein, M.D., assistant professor of obstetrics and gynecology and women's health, who will lead this research. “So we are trying to determine the epigenetic changes in these babies that make them more susceptible to chronic disease and premature death.”

    The researchers hypothesize that conditions during fetal development alter epigenetic patterns of DNA methylation in stem cells. These changes may be a marker for or contribute to susceptibility to type 2 diabetes and other age-related diseases.

    The second grant of $1.49 million, which will span four years, will address the epigenetic landscape of chronic kidney disease. The researchers suspect that unfavorable environmental conditions such as poor nutrition during pregnancy can imprint abnormal DNA methylation patterns on the fetal kidney.

    Epigenetic changes may also explain why diabetes is the leading cause of renal failure, the scientists note. “People with diabetes who control blood glucose levels develop fewer complications,” says Katalin Susztak, M.D., Ph.D., associate professor of medicine, and leader of this grant. “But they still face a greater risk for kidney failure and other complications, probably because their bodies remember periods from long ago when their glucose was not well controlled. We want to learn whether this so-called hyperglycemic memory is coded in DNA methylation patterns.”

     



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