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editorial
. 2019 Jan;104(1):3–6. doi: 10.3324/haematol.2018.205989

Figure 1.

Figure 1.

The mechanism of thrombus formation in myeloproliferative neoplasm. The Jak2V617F mutation causes an increase in endothelial cell (EC) Weibel-Palade body (WPB) degranulation of P-selectin and von Willebrand factor (VWF); translocation of Rap1 towards the cell membrane with activation of the integrins LFA1 and VLA4; and increased neutrophil extracellular trap (NET) formation. In addition, a red blood cell-platelet interaction through FasL/FasR causes externalization of phosphatidylserine (PS). All of these events play a role in thrombus formation. Rap1: Ras-related protein 1; LFA1: lymphocyte function-associated antigen 1; STAT: signal transducer and activator of transcription; PAD4: peptidyl arginine deimidase 4; ICAM-1: intracellular adhesion molecule 1; VCAM-1: vascular cell adhesion molecule 1; VLA4: very late antigen-4: FasL: Fas ligand.