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. Author manuscript; available in PMC: 2020 Jan 1.
Published in final edited form as: Cell Signal. 2018 Oct 16;53:246–255. doi: 10.1016/j.cellsig.2018.10.010

Figure 5. HDAC6 inhibition suppresses PM-induced IL-6 increase and STAT3 activation.

Figure 5.

A - Human pulmonary EC were pre-treated with HDAC6 inhibitor TubA (10 μM), JAK inhibitor I (5 μM) or Rho inhibitor Y27632 (2 μM) for 30 min followed by treatment with PM (20 μg/cm2, 1 hr). Western blot assay using phospho-STAT3 antibody was performed to detect phosphoSTAT3 levels. B - Cells transfected with non-specific or HDAC6-specific siRNA were stimulated with PM (20 μg/cm2, 1 hr), and phospho-STAT3 levels were evaluated by western blot assay was performed to determine phospho-STAT3 levels. HDAC6 knockdown was confirmed by probing with HDAC6 antibody and α-Tubulin served as loading control. Bar graphs depict quantitative densitometry analysis of western blot experiments; n=3; **p<0.05. Data are expressed as mean + SD. C - IL-6 levels in the EC conditioned medium after 6-hr stimulation with PM were detected by ELISA assay. Data are presented as mean ± S.D.; n=6, *p<0.05.