fig6

Mitochondrial DAMPs-dependent inflammasome activation during aging induces vascular smooth muscle cell dysfunction and aortic stiffness in low aerobic capacity rats

Figure 6. Rapamycin or MitoTEMPO treatment inhibited inflammasome activation in VSMCs from old LCR rats. Representative Western blots of inflammasome marker proteins of VSMCs treated with or without DAMPs (A). Densitometric quantification of proteins expressed as fold change ± SEM, n = 4 independent cell lines (B). Representative Western blots of inflammasome markers in VSMC lysates were isolated after 16 h of 20 nM rapamycin treatment (C). Densitometric quantification of protein levels expressed as fold change ± SEM, n = 4 (D). Representative Western blots of inflammasome markers in VSMC lysates after 16 h of 10 nM MitoTEMPO treatment (E). Densitometric quantification of protein levels expressed as fold change ± SEM, n = 4 (F). Estimation of circulating mitochondrial DNA with MTCO1 specific-Taqman probe using qPCR. Data are Ct values (Mean ± SEM, n = 3-4) (G). Representative Western blots of p202 protein levels in VSMC lysates with and without rapamycin or MitoTEMPO treatments (H). Densitometric quantification of protein levels expressed as fold change ± SEM, n = 4. (I). *P < 0.05; **P < 0.01.

The Journal of Cardiovascular Aging

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