Fig. 8
HDAC6i decreases proplatelet formation through CTTN hyperacetylation. a, b Western blot analysis and quantification showing the hyperacetylation of CTNN in MKs treated for 48 h with HDAC6 inhibitors (ACY1215 or Tubastatin) compared to untreated MKs. c, d HDAC6 knockdown with shRNA increases CTTN acetylation level. e, f Expression of a CTTN-9KR, a non-acetylable form of CTNN reversed the PPF decrease induced by both HDAC6i (e) and by shHDAC6 (f). Results are representative of three independent experiments (n = 3). Unpaired Student’s t test *p < 0.05; **p 0.001; ***p < 0.0001. g, h Hyperacetylated CTTN decreases F-actin in MKs. g MKs transduced with either an empty vector or a lentivirus encoding deacetylated CTTN mimic (CTTN-9KR) were sorted, then treated for 48 h with either 1 μM of Tubastatin A or ACY1215. G and F actin were both separated by ultracentrifugation and lysates were analyzed by western blot. h Quantification of western blotting experiments from two independent experiments. Error bars are SEM
