PHOENIX, Ariz.-- April 22, 2011-- A gene called PVT1 may help reduce the kidneys ability to filter blood, leading to kidney disease, kidney failure and death, according to a study published today by researchers at the Translational Genomics Research Institute (TGen).
The TGen team found PVT1 expression levels increased up to 5-fold in response to hyperglycemia, or high blood sugar, a condition that often accompanies diabetes.
But by knocking down or reducing the expression of the PVT1gene, TGen researchers lowered the amount of proteins associated with the excessive accumulation of extracellular matrix (ECM) in glomeruli, part of the basic filtration unit of kidneys, according to the TGen study published today in the online scientific journal Public Library of Science (PLoS) ONE.
The accumulation of excessive ECM within the mesangial cells, which regulate blood flow in capillaries inside the kidney, is a hallmark of diabetic nephropathy, or kidney disease, which is the leading cause of reduced life expectancy among the nation's growing numbers of diabetics.
"The goal of this study was to identify possible molecular mechanisms by which PVT1 may contribute to the development and progression of diabetic nephropathy in mesangial cells," said Dr. Johanna DiStefano, the study's senior author and Director of TGen's Diabetes, Cardiovascular and Metabolic Diseases Center.
"Despite the growing magnitude of the disease, the molecular mechanisms underlying the etiology of diabetic nephropathy remain poorly understood," Dr. DiStefano said.
PVT1, also known as plasmacytoma variant translocation 1, was previously identified by Dr. DiStefano's team as a candidate gene for End Stage Renal Disease (ESRD), or kidney failure. Too much PVT1 also has been associated with breast and ovarian cancers, in which it may help cause cells to multiply out of control and fail to go through the normal process of cellular death.
|Contact: Steve Yozwiak|
The Translational Genomics Research Institute