So far, the antiviral mechanism of Mx protein has been not known completely, although the triple GTP-binding region is an indispensable part for Mx protein and GTP activity is essential for playing its antiviral function. Mx proteins inhibit a variety of negative-strand RNA viruses. Different Mx proteins have different anti-viral specificity and the antiviral mechanisms are also slightly different. Mx protein located in the nucleus can inhibit the replication of the influenza virus in mice. However, Mx A can block the virus into the cytoplasm and prevent viral nucleocapsid getting into the nucleus, and inhibiting virus replication in the nucleus. The anti-VSV mechanism of Mx A protein was to inhibit viral transcription initiation stage by blocking RNA primer and mRNA synthesis. Similarly, cytopathic inhibition assay showed that CEF cells transfected with Mx gene demonstrated antiviral activity and CEF cells couldn’t be infected by NDV within 48 h, which indicated that Mx protein was expressed by CEF cells. Mx plays its antiviral activity by inhibition of its replication. In summary, both Mx and NA proteins have the ability to resist the virus infection, it will be a desirable antiviral pathway if both of genes could be combined together. This study indicated that MxNA co-transfection group prolonged significantly the CEF cells resistance against viral infection; there was no pathological change within the first 72 h of infection, which was significantly better than lonely Mx gene group or NA gene group. These results suggest that Mx protein inhibit viral replication while NA proteins prevent the virus releasing from the cell and infecting other cells, demonstrating that there are synergistic antiviral effects between Mx gene and NA gene. However, the intrinsic antiviral mechanisms between these two genes need to be further explored. Microparticles are small fragments generated from the plasma membrane after cell AbMole Simetryn stimulation. The composition of MPs and the messages they transport can differ depending on their origin. MPs can be engineered to over-express different proteins by driving the synthesis of the relevant protein in MP-producing cells. We have demonstrated that MPs released by apoptotic/stimulated human T lymphocytes harbor the morphogen Sonic hedgehog and improve endothelial function in the mouse aorta by increasing NO release. Also, endothelial dysfunction in mouse coronary artery after ischemia/reperfusion can be prevented by treatment with Shh-carrying MPs. Moreover, MPs expressing Shh favor in vitro angiogenesis and the recovery of hindlimb flow after peripheral ischemia through the activation of endothelial NO synthase and the increase of NO release and 
pro-angiogenic factor production. The present study further aims to investigate whether MPs bearing Shh may correct Ang II-induced hypertension and endothelial dysfunction in mice.