Blood: two adjustment factors for vWF maturation and release: vesicles and BLOC-2

The !---- vascular hemophilia factor (vWF) is a necessary hemostatic protein that is synthesized in endothelial cells and stored in the Weibel-Palade small body (WPB)understanding the potential mechanisms of WPB biooccurrence and cytospitation can achieve therapeutic regulation of endogenous vWF, but the best target for regulatable vWF release has not yet been identifiedGiven that the biosynthesis of lysozymatic-related organ2 (BLOC-2) can be shipped in the biosynthesis of platelet-dense particles and melanin, like WPB, it is the lysosome-related organelle (LRO)Sharda and others assume that BLOC-2-dependent lysosome transport is critical to the occurrence of WPB organisms and attempts to identify proteins that interact with BLOC-2bloc-2 depletion causes the direction error of the transport tube carrying goods from the inner body, which causes WPBs to lack the internal input and not matureidentified by immunoprecipitation as a combination partner of BLOC-2depleted vesicle complex can replicate the surface of bloc-2 depletion, resulting in WPB immaturityin addition, the process of releasing immature WPB from BLOC-2 or vesicle-depleted endothelial cells lacks vWF in the form of a high molecular weight, demonstrating the importance of bloc-2/vesicle-mediated endothelial input during vWF maturationHowever, BLOC-2 and vesicles show very different effects on vWF releasealthough bloc-2 depletion will damage the role of cytospit, but vesicle depletion will increase wpB's cytospit effect, indicating that the vesicles are used to play the pliersEndosidin2 (endorphin 2), it is possible to irreversibly increase the secretion of mature WPBs containing high molecular weight forms vWFthis study shows that although BLOC-2 and vesicles are synergistic in the formation of WPB, only vesicles can prevent WPB releasethe role of vesicles in vWF maturation and release is separable, or can be used to target the vesicles to increase vWF release