Although it was published before that HUVEC marker expression changed via IVSWT, we could not confirm these data in our study. This may be due to cell donor variability or shockwave device specialities. Our results Erdosteine further demonstrated that podoplanin, a LEC-specific marker, was significantly upregulated after IVSWT. Since two cell populations differing in size and podoplanin expression became visible during the analyses, we investigated these different sub-groups in more detail. Interestingly, IVSWT mediated a morphology change which led to a visible shift from the podoplaninlow larger cells to the podoplaninhigh smaller population. However, both populations had the same induction of podoplanin after IVSWT, indicating that the total increase of podoplanin is merely based on the population shift and increase in the amount of podoplaninhigh cells. Further marker expression analyses revealed that other panendothelial and Mesna lymphatic specific markers on LECs are unaffected by IVSWT indicating the IVSWT act on distinct cell functions and does not show an universal increase of markers or cell functions in contrast to published data. Moreover, the importance of choosing the optimal stimulation parameters mentioned before was enforced by showing a strong energy flux density dependence of podoplanin upregulation in LECs and cell type specificity since HUVECs showed different responses than LECs. The IVSWT-promoted population shift of LECs revealed several differences in the transcriptome. By comparing both subpopulations of LECs we found several genes up- and downregulated. Interestingly, there was no difference in the expression of podoplanin on the mRNA level, suggesting posttranscriptional or translational regulation by shockwaves. VWF expression differed comparing the podo plan in high with the podo plan in low populations. It has been shown before that shear stress mediates an upregulation of vWF in late endothelial progenitor cells suggesting that IVSWT may have similar effects on LECs. This could be explained by concomitant down-regulation of several miRNAs, which are predicted to target vWF.