The heat that hurts pg. 2
In one of their highest profile papers, published in the journal Science in 1995, Fazio, Linton and James Atkinson, M.D., Ph.D., professor of Pathology, reported that apolipoprotein E (apoE), a protein important in lipoprotein metabolism, seemed to protect mice from developing atherosclerosis.
The largest supply of apoE comes from the liver, Linton says. But the protein is also made by macrophages, and thus may participate in the inflammatory response.
To determine what, if any, role apoE expressed in macrophages played in the development of atherosclerosis, Linton and Fazio studied a strain of mice that lacked both copies of the apoE gene. These mice develop significant atherosclerosis, unlike their genetically normal—or wild type—counterparts. The researchers irradiated the apoE deficient mice to kill their bone marrow, the source of macrophages, then gave them transplants of bone marrow cells from wild type mice.
Mice deficient in apoE that received the transplants did not develop atherosclerotic plaques. “The small amount of apoE that came from the bone marrow was enough to cure the mice,” says Linton.