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Specific protein may increase risk of blood-vessel constriction linked to gum disease

Date:
April 18, 2012
Source:
American Heart Association
Summary:
A protein involved in cellular inflammation may increase the risk of plaque containing blood vessels associated with inflammatory gum disease, according to new research.

A protein involved in cellular inflammation may increase the risk of plaque containing blood vessels associated with inflammatory gum disease, according to research presented at the American Heart Association's Arteriosclerosis, Thrombosis and Vascular Biology 2012 Scientific Sessions in Chicago.

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The protein, CD36, is found in blood cells, as well as many other cell types. Research has shown that CD36 may increase the harmful effects of "bad cholesterol," or low-density lipoprotein (LDL).

Investigators "knocked out," or deleted, the gene responsible for CD36 production, then induced plaque in blood vessels by feeding mice a high fat diet. Some animals were also infected with the bacteria associated with gum disease.

More fatty plaque accumulation occurred in the blood vessels of the animals that were infected with gum disease. In the animals with the deleted CD36 gene, however, vessels remained free of new plaque even when oral inflammation occurred.


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The above story is based on materials provided by American Heart Association. Note: Materials may be edited for content and length.


Cite This Page:

American Heart Association. "Specific protein may increase risk of blood-vessel constriction linked to gum disease." ScienceDaily. ScienceDaily, 18 April 2012. <www.sciencedaily.com/releases/2012/04/120418162252.htm>.
American Heart Association. (2012, April 18). Specific protein may increase risk of blood-vessel constriction linked to gum disease. ScienceDaily. Retrieved December 19, 2014 from www.sciencedaily.com/releases/2012/04/120418162252.htm
American Heart Association. "Specific protein may increase risk of blood-vessel constriction linked to gum disease." ScienceDaily. www.sciencedaily.com/releases/2012/04/120418162252.htm (accessed December 19, 2014).

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