Fig. 6From: NFATc2-dependent epigenetic upregulation of CXCL14 is involved in the development of neuropathic pain induced by paclitaxelIncreased interactions between NFATc2 and p300 increased the level of acetylated histone H4 on the special region area of CXCL14 promoter. a Six potential motif for NFATc2 binding on CXCL14 promoter. b ChIP-PCR assay was performed with CXCL14 antibody on day 5 and day 10 after paclitaxel treatment in rats using different primer (**P < 0.01 vs vehicle, n = 5 per group). c NFATc2 was significantly increased in immunocomplex precipitated by p300 antibody on day 10 after paclitaxel treatment (**P < 0.01 vs the vehicle group, n = 4 per group). d p300 content was increased precipitated by NFATc2 antibody following paclitaxel treatment on day 10 (**P < 0.01 vs the vehicle group, n = 4 per group). e Western blotting showed that the acetylation of H4 significantly increased on day 5 and day 10 after application of paclitaxel (**P < 0.01 vs the vehicle group, n = 4 per group). f Application of paclitaxel did not change the acetylation of H3 in dorsal horn (n = 4 per group). g H4 acetylation on the NFATc2 binding region in CXCL14 promoter was enhanced on day 10 after application of paclitaxel (**P < 0.01 vs the vehicle group, n = 5 per group). h Intrathecal application of FK506 (NFATc2 inhibitor) decreased the increase of H4 acetylation on CXCL14 promoter on day 10 following paclitaxel application (**P < 0.01 vs the vehicle group, ##P < 0.01 vs the paclitaxel treatment, n = 5 per group)Back to article page