Deleting a protein might reduce cardiovascular disease
Deleting the TRPM2 protein from macrophages reduced atherosclerosis in
mice

Date:
March 28, 2022
Source:
University of Connecticut
Summary:
Macrophages travel through our arteries, gobbling fat. But
fat-filled macrophages can narrow blood vessels and cause heart
disease. Now, researchers describe how deleting a protein could
prevent this and potentially prevent heart attacks and strokes
in humans.



FULL STORY ========================================================================== Macrophages travel through our arteries, gobbling fat. But fat-filled macrophages can narrow blood vessels and cause heart disease. Now,
UConn Health researchers describe in Nature Cardiovascular Research
how deleting a protein could prevent this and potentially prevent heart
attacks and strokes in humans.


========================================================================== Macrophages are large white blood cells that cruise through our body as
a kind of clean-up crew, clearing hazardous debris. But in people with atherosclerosis -- fatty deposits and inflammation in their blood vessels
-- macrophages can cause trouble. They eat excess fat inside artery walls,
but that fat causes them to become foamy. And foamy macrophages tend to encourage inflammation in the arteries and sometimes bust apart plaques, freeing clots that can cause heart attack, stroke or embolisms elsewhere
in the body.

Changing how macrophages express a certain protein could prevent that kind
of bad behavior, reports a team of researchers from UConn Health. They
found that the protein, called TRPM2, is activated by inflammation. It
signals macrophages to start eating fat. Since inflammation of the
blood vessels is one of the primary causes of atherosclerosis, TRPM2
gets activated quite a bit. All that TRPM2 activation pushes macrophage activity, which leads to more foamy macrophages and potentially more
inflamed arteries. The way that TRPM2 activated macrophage activity was surprising, says Lixia Yue, a UConn School of Medicine cell biologist.

"They form a vicious cycle promoting the development of atherosclerosis,"
Yue says.

Yue and Pengyu Zong, a graduate student and the first author of
the paper, demonstrated one way to stop the cycle, at least in
mice. They deleted TRPM2 from a type of lab mouse that tends to get atherosclerosis. Deleting that protein didn't seem to hurt the mice,
and it prevented the macrophages from getting foamy. It also alleviated
the animals' atherosclerosis.

Now Yue and Pengyu Zong, and the rest of the team are looking at whether increased TRPM2 expression in monocytes (precursors of macrophages)
in the blood correlates with severity of cardiovascular disease in
humans. If they find that there is a correlation, high levels of TRPM2
might be a risk marker for heart attack and stroke.

This research was funded by grants from the American Heart Association
and the National Institutes of Health National Heart, Lung and Blood
Institute.


========================================================================== Story Source: Materials provided by University_of_Connecticut. Original
written by Kim Krieger. Note: Content may be edited for style and length.


========================================================================== Journal Reference:
1. Pengyu Zong, Jianlin Feng, Zhichao Yue, Albert S. Yu, Jean Vacher,
Evan
R. Jellison, Barbara Miller, Yasuo Mori, Lixia Yue. TRPM2 deficiency
in mice protects against atherosclerosis by inhibiting TRPM2-CD36
inflammatory axis in macrophages. Nature Cardiovascular Research,
2022; DOI: 10.1038/s44161-022-00027-7 ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2022/03/220328111741.htm

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