• Deleting a protein might reduce cardiova

    From ScienceDaily@1:317/3 to All on Monday, March 28, 2022 22:30:40
    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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