Research Paper Volume 12, Issue 6 pp 5411—5422

HDAC6 promotes sepsis development by impairing PHB1-mediated mitochondrial respiratory chain function

Figure 5. HDAC6 inhibits the expression of PHB1 and causes subsequent mitochondrial dysfunction. U937 cells were infected with an HDAC6–expressing or HDAC6-specific shRNA–expressing lentivirus, and then gene expression and the mitochondrial respiratory control rate were determined to evaluate the influence of HDAC6 on mitochondrial function. (A) HDAC6 mRNA and protein expression; (B) PHB1 mRNA and protein expression; and (C) the mitochondrial respiratory control rate in lenti-HDAC6 (HDAC6 overexpressing) and lenti-sh-HDAC6 (HDAC6 knockdown) U937 cells. (D) The mitochondrial respiratory control rate in HDAC6 agonist (ITSA1) and HDAC6 inhibitor (Tri A) treated macrophages. Results are expressed as the mean ± SEM. **P < 0.01.