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Lust et al. Vessel Plus 2021;5:7 I http://dx.doi.org/10.20517/2574-1209.2020.52 Page 9 of 14

Figure 3. Impact of elevated pressure levels on markers of cell activity. Isolated branches of the mesenteric vein of male NMRI mice
were exposed to 4- or 16-mmHg, respectively in the presence or absence of diclofenac. Protein extracts generated from these blood
vessels were analyzed by capillary electrophoresis as described above. The level of phosphorylated ERK1/2 and the abundance of MMP-
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2 (pro-enzyme: 72 kDa was below detection limit, active form: ~ 62 kDa) were determined; A: *P < 0.05 vs. 4 mmHg, P < 0.05 vs. 16
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mmHg, n = 4-5 as indicated; B: **P < 0.01 vs. 4 mmHg, P < 0.01 vs. 16 mmHg, n = 3-4 as indicated.
In this study, we have verified both COX-1 and COX-2 protein expression in isolated and cannulated
branches of mesenteric mouse veins whose RNA expression was slightly, but not significantly increased
after elevating the intraluminal pressure for several hours. In vivo, COX-2 was barely detectable in
quiescent auricle veins but was abundant in endothelial cells of remodeling veins. Although the regulatory
determinants remain obscure, upregulation of COX-2 under these conditions correlates with the induction
of biomechanical stress, which is shown to drive COX-2 expression in human endothelial cells in this and
prior studies . However, while the presence of COX may further result in the production of PGH2, the
[15]