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. Author manuscript; available in PMC: 2021 Dec 1.
Published in final edited form as: Hypertension. 2020 Oct 5;76(6):1787–1799. doi: 10.1161/HYPERTENSIONAHA.120.16118

Figure 3. The release of HMGB1 dimer from HPASMC is mitochondrial ROS dependent.

Figure 3.

HPASMC but not HPAEC death induces a release of HMGB1 in a dimeric form (A, N=5). The elevated production of reactive oxygen species (ROS), such as hydrogen peroxide (H2O2, B, N=8) or mitochondrial superoxide (O2−, C, N=8) found in HPASMC versus HPAEC, could be responsible for the oxidation of HMGB1 into dimers. However, attenuation of H2O2 levels by pretreatment HPASMC with NOX1/4 inhibitor, GKT137831, did not alter HMGB1 dimer/monomer levels in cells (D, N=6–8). In contrast, incubation of HPASMC in mitochondria-specific O2− scavenger, MitoTempol, reduced not only the levels of mitochondrial ROS but also HMGB1 dimer/monomer ratio (E, N=6–8). Data presented as Mean±SEM, *P<0.05, **P<0.01, ***P<0.001 vs. untreated Control; §P<0.05, §§§P<0.001 vs. necrosis in HPASMC.