Accession Number : AD1050236

Title :   Control of Atherosclerosis Regression by PRMT2 in Diabetes

Descriptive Note : Technical Report,01 Aug 2016,31 Jul 2017

Corporate Author : New York University School of Medicine New York United States

Personal Author(s) : Fisher, Edward

Full Text :

Report Date : 01 Aug 2017

Pagination or Media Count : 10

Abstract : Diabetics have more heart disease than their non-diabetic counterparts, even though drugs like statins are equally effective in both groups at lowering the blood levels of harmful cholesterol. We have identified an enzyme called PRMT2, which regulates the abundance of a cellular cholesterol transporter that helps to prevent cells from accumulating in arteries and forming a plaque. We have shown that the level of PRMT2, while high in healthy cells, is very low in cells from diabetics when blood sugar levels are elevated. Because PRTM2 isnt around in cells under diabetic conditions, we predict that more cells accumulate in the artery, thus allowing the plaque to grow and exacerbating heart disease in diabetics. To test this, we will determine what happens to the growth of a plaque in an artery when we eliminate PRMT2 with and without diabetes in mouse models of heart disease. We expect that plaques will grow larger in the absence of PRMT2. To better understand how PRMT2 suppresses plaque growth, we will also identify proteins that are modified by PRMT2 in cells from the plaque and determine if these proteins participate in plaque formation. Given that we also dont understand why PRMT2 levels decrease in diabetes, we will identify cellular proteins that regulate PRMT2 levels. That knowledge might enable us to develop ways to restore the normal level of PRMT2 in diabetes, and prevent the cells from contributing to plaque formation, and reduce heart attacks.

Descriptors :   heart diseases , sclerosis , diabetes , enzymes , proteins , macrophages , transcription (genetics) , Bone Marrow

Subject Categories : Medicine and Medical Research
      Genetic Engineering and Molecular Biology

Distribution Statement : APPROVED FOR PUBLIC RELEASE