To understand the effect of platelet membrane glycoprotein (GP) Ⅱ b / Ⅲ a on the expression of matrix metalloproteinase (MMP-2, 9) mRNA. Methods: Human umbilical vein endothelial cells were cultured in vitro, and MMP-2, -9 activity and mRNA expression were detected by zymography and reverse transcription polymerase chain reaction (RT-PCR). After the cells are fused into a single layer, add serum-free medium, platelets at rest, activated platelets and interleukin-1β (IL-β). After 60 minutes of co-cultivation, wash the platelets off and continue culturing endothelial cells 6 h. The supernatant and cells were used to detect the activity of MMP-2 and MMP-9 by zymography, respectively, and RT-PCR analysis of mRNA expression. Results: After endothelial cells were co-cultured with activated platelets, zymography showed that compared with the control group, unactivated platelets slightly induced MMP-2 and MMP-9 secretion (P <0.05), while activated platelets could Significantly induce the secretion of these two (P <0.01), which is equivalent to the role of IL-1β; and the activated form of 62 kDaMMP-2 can also be seen. After adding the blocking agent GRGDSP and GPⅡb / Ⅲa monoclonal antibody (7E3), it was found that the secretion of MMP-2 and MMP-9 was reduced. The expression of uPAR and MT1-MMP on the surface of endothelial cells co-cultured with activated platelets and MMP-2 mRNA in the supernatant was significantly increased compared with the control group (P <0.01), while the resting platelet effect was not significant . After adding GRGDSP or 7E3, mRNA expression decreased. Conclusion: (1) The activated platelets have the same effect as IL-β, which can significantly induce the secretion of MMP-2 and MMP-9; it can significantly increase the expression of uPAR, MT1-MMP and MMP-2 mRNA in the supernatant ; (2) GPⅡb / Ⅲa blockers may inhibit a series of inflammatory reactions such as platelet aggregation and adhesion in unstable plaque sites.
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