Blood: RGS10 and RGS18 work together to limit unnecessary platelet activation

G protein conjugate receptor sishose activation is a key medium, and its signaling can be regulated by members of the G protein signal (RGS) family regulatorThe two most abundant RGS proteins in human and mouse platelets are RGS10 and RGS18Although both proteins have been independently studied, there are still critical questions about the overall effectofs of this regulation on plateletsrecently, researchers found that platelet survival in mice with both proteins missing decreased, and platelet counts decreased by 40 percent, a phenomenon that can be partially reversed by aspirin and P2Y12 antagoniststhe underlying TLT-1 expression of these platelets increased, the dose/reaction curve of the clotting enzyme receptor-activated peptide shifted to the left, the maximum reaction to ADP and TxA2 increased, and the response to penetrating damage in the body was significantly amplifiedknocking out one of the two genes alone does not show this performanceIn vitro, RGS10-/-platelets respond more to agonists, but platelet counts and survival rates are normalRGS18-/- Mice had a 15% reduction in platelets and were not affected by antiplatelet drugs, and the response to platelet agonists was almost normal and platelet survival was normalIn all three mouse lineages (double knock and two single knocks), the number and multiplicity of macronuclear cells were normal, but in RGS18-//-and RGS10-/---18-/-- - In mice, the eastern acute platelet reduction was slower, these results show that RGS10 and RGS18 complement each other in plateletsIn addition, the study also revealed that the regulatory mechanism in the body to control platelet reaction, regulate the hemostatic response to injury, promote platelet production and prolong platelet survival