Concepts familiar from grade-school algebra have broad ramifications in computer science.
CAMBRIDGE, Mass.--Atherosclerosis, the leading cause of death in Western
industrialized countries, is characterized by the build-up of
cholesterol and similar fatty compounds on the walls of the arteries.
The risk of developing the disease depends in large measure on the
relative amount of two particles, called lipoproteins, which carry
cholesterol through the bloodstream.
One of these, low density lipoprotein (LDL), is known as "bad
cholesterol" because the risk for atherosclerosis increases as the
amounts of LDL in the blood increase. The other, high density
lipoprotein (HDL), is called "good cholesterol" because the more you
have in your blood, the lower the risk. These lipoproteins perform many
functions in the body, including transporting cholesterol to tissues
that convert cholesterol to steroid hormones--important regulators of
many key body functions.
A team of biomedical scientists at the Massachusetts Institute
Technology and Southwestern Medical Center reports in the current issue
of Science magazine (Jan. 26, 1996) the first identification of a cell-
surface receptor for HDL. An accompanying commentary calls the
identification of this receptor "an important advance" toward
understanding the metabolism of HDL.
About 21 years ago, Professors Michael Brown and Joseph Goldstein
at the Southwestern Medical Center reported their discovery of a
receptor for LDL. Their landmark discovery and subsequent investigations
of LDL receptors has provided major insights into basic mammalian cell
biology, lipid metabolism and atherosclerosis.
Until now, and despite extensive efforts by many laboratories, a
well characterized HDL receptor had not been found. The identification
and analysis of this new HDL receptor, along with ongoing studies of HDL
metabolism throughout the world, may eventually provide insights into
the mechanisms by which HDL lowers the risk of atherosclerosis and
provides cholesterol for steroid hormone synthesis.
The authors of the Science paper are Susan Acton, Attilio Rigotti,
Katherine T. Landschulz, Shangzhe Xu, Helen H. Hobbs and Monty Krieger.
Drs. Acton and Rigotti, along with Mrs. Xu, were members of Professor
Krieger's laboratory in the Department of Biology at MIT. Dr. Landschulz
worked with Professor Hobbs in the Departments of Internal Medicine and
Molecular Genetics at the University of Texas Southwestern Medical
Center in Dallas.
Professor Krieger cautions, "Much work remains to be done before we
will be able to clearly define this new receptor's role in HDL
metabolism and determine if it participates in metabolic pathways
related to atherosclerosis and steroid hormone synthesis."
The research was supported by grants from the National Institutes
of Health Heart Lung and Blood Institute (HL41484, HL52212, HL09047 and
HL20948), The Perot Family Fund, and a Howard Hughes Medical Institute
Postdoctoral Fellowship to Dr. Rigotti.