Atherosclerosis Researcher at Geisel Receives NIH Grant


Read the full story by Matthew Wiencke, published by the Geisel School of Medicine.

Geisel School of Medicine post-doctoral researcher Elaina Melton has received the National Institutes of Health (NIH) Ruth L. Kirschstein National Research Service Award (NRSA) from the National Heart, Lung, and Blood Institute (NHLBI) to support her research on two cholesterol-related diseases, atherosclerosis and xanthomatosis.

Elaina Melton is a post-doctoral researcher at the Geisel School of Medicine. She works in Professor of Biochemistry Ta-Yuan Chang’s lab. (Photo courtesy of the Geisel School of Medicine)

“This is an important and prestigious fellowship that will help Elaina Melton to become an independent investigator in the near future,” says Ta-Yuan Chang, a professor of biochemistry at Geisel. Melton was awarded the fellowship “on her first try which is very rare for these kinds of awards,” Chang says. Melton is a postdoctoral researcher in Chang’s lab.

The NRSA provides funding for up to three years for promising early-stage postdoctoral researchers who have the potential to become independent investigators in health-related research projects. The NHLBI is committed to training and mentoring emerging scientists and physicians seeking the cause of disease and enables the translation of basic discoveries into clinical practice. Melton’s research will be funded for two years.

Chang has spent many years studying the role that the gene ACAT1 plays in multiple human diseases, including Alzheimer’s and atherosclerosis, a hardening of the arteries due to buildup of plaque. ACAT1 catalyzes the conversion of cholesterol into a storable form called cholesterol esters. A buildup of cholesterol esters in macrophages (white blood cells) within an aortic lesion is a hallmark of atherosclerosis. Melton is studying the effects of inactivating ACAT1 in macrophages on the progression of atherosclerosis. Her research involves the use of atherosclerosis mouse models engineered to be born with or without the ACAT1 gene in their macrophages.

“We are putting macrophage-specific ACAT1-knockout mice on a high cholesterol diet to induce atherosclerosis,” Melton explains. “We’ll then characterize the atherosclerotic plaque by assessing plaque size and composition.” Her findings will give deeper insight into how ACAT1 is involved in atherosclerosis.

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