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- W2036729274 abstract "Platelet secretion not only drives thrombosis and hemostasis, but also mediates a variety of other physiological and pathological processes. The ubiquitous SNARE machinery and a number of accessory proteins have been implicated in regulating secretion in platelet. Although several platelet SNAREs have been identified, further members of the SNARE family may be needed to fine-tune platelet secretion. In this study we identified expression of the t-SNARE syntaxin 8 (STX8) (Qc SNARE) in mouse and human platelets. In mouse studies, whereas STX8 was not essential for α-granule or lysosome secretion, Stx8−/− platelets showed a significant defect in dense granule secretion in response to thrombin and CRP. This was most pronounced at intermediate concentrations of agonists. They also showed an aggregation defect that could be rescued with exogenous ADP and increased embolization in Stx8−/− mice in vivo consistent with an important autocrine and paracrine role for ADP in aggregation and thrombus stabilization. STX8 therefore specifically contributes to dense granule secretion and represents another member of a growing family of genes that play distinct roles in regulating granule release from platelets and thus platelet function in thrombosis and hemostasis.BackgroundThe molecular machinery controlling exocytosis of the three secretable granules types in platelets is not fully elucidated.ResultsATP secretion, aggregation, and thrombus stability are defective in Stx8−/− mouse platelets.ConclusionSTX8 is involved in platelet dense granule secretion, and the STX8-mediated pathway contributes to thrombus stabilization.SignificanceIdentification of the novel functional SNARE STX8 suggests alternative mechanisms of granule secretion exist in platelets. Platelet secretion not only drives thrombosis and hemostasis, but also mediates a variety of other physiological and pathological processes. The ubiquitous SNARE machinery and a number of accessory proteins have been implicated in regulating secretion in platelet. Although several platelet SNAREs have been identified, further members of the SNARE family may be needed to fine-tune platelet secretion. In this study we identified expression of the t-SNARE syntaxin 8 (STX8) (Qc SNARE) in mouse and human platelets. In mouse studies, whereas STX8 was not essential for α-granule or lysosome secretion, Stx8−/− platelets showed a significant defect in dense granule secretion in response to thrombin and CRP. This was most pronounced at intermediate concentrations of agonists. They also showed an aggregation defect that could be rescued with exogenous ADP and increased embolization in Stx8−/− mice in vivo consistent with an important autocrine and paracrine role for ADP in aggregation and thrombus stabilization. STX8 therefore specifically contributes to dense granule secretion and represents another member of a growing family of genes that play distinct roles in regulating granule release from platelets and thus platelet function in thrombosis and hemostasis. The molecular machinery controlling exocytosis of the three secretable granules types in platelets is not fully elucidated. ATP secretion, aggregation, and thrombus stability are defective in Stx8−/− mouse platelets. STX8 is involved in platelet dense granule secretion, and the STX8-mediated pathway contributes to thrombus stabilization." @default.
- W2036729274 created "2016-06-24" @default.
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- W2036729274 date "2015-01-01" @default.
- W2036729274 modified "2023-10-16" @default.
- W2036729274 title "Syntaxin 8 Regulates Platelet Dense Granule Secretion, Aggregation, and Thrombus Stability" @default.
- W2036729274 cites W1547732923 @default.
- W2036729274 cites W1588101416 @default.
- W2036729274 cites W1634711419 @default.
- W2036729274 cites W176610512 @default.
- W2036729274 cites W1964607696 @default.
- W2036729274 cites W1965253809 @default.
- W2036729274 cites W1966503198 @default.
- W2036729274 cites W1967533589 @default.
- W2036729274 cites W1971124929 @default.
- W2036729274 cites W1978605633 @default.
- W2036729274 cites W1979438759 @default.
- W2036729274 cites W1995601334 @default.
- W2036729274 cites W2006634074 @default.
- W2036729274 cites W2008920235 @default.
- W2036729274 cites W2010327987 @default.
- W2036729274 cites W2015713712 @default.
- W2036729274 cites W2016236015 @default.
- W2036729274 cites W2027517877 @default.
- W2036729274 cites W2028689554 @default.
- W2036729274 cites W2042212641 @default.
- W2036729274 cites W2047164801 @default.
- W2036729274 cites W2048837254 @default.
- W2036729274 cites W2049751046 @default.
- W2036729274 cites W2050267141 @default.
- W2036729274 cites W2051506039 @default.
- W2036729274 cites W2052394407 @default.
- W2036729274 cites W2055882936 @default.
- W2036729274 cites W2056499061 @default.
- W2036729274 cites W2058742122 @default.
- W2036729274 cites W2059566494 @default.
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- W2036729274 cites W2079859456 @default.
- W2036729274 cites W2085680244 @default.
- W2036729274 cites W2095351157 @default.
- W2036729274 cites W2103638366 @default.
- W2036729274 cites W2109503431 @default.
- W2036729274 cites W2124422993 @default.
- W2036729274 cites W2128913650 @default.
- W2036729274 cites W2129271267 @default.
- W2036729274 cites W2130785214 @default.
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- W2036729274 cites W2137163623 @default.
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- W2036729274 doi "https://doi.org/10.1074/jbc.m114.602615" @default.
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