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Fig. 6 | Journal of Neuroinflammation

Fig. 6

From: NFATc2-dependent epigenetic upregulation of CXCL14 is involved in the development of neuropathic pain induced by paclitaxel

Fig. 6

Increased 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)

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