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Fig. 1 | Clinical Epigenetics

Fig. 1

From: A DNA methylation signature in the stress driver gene Fkbp5 indicates a neuropathic component in chronic pain

Fig. 1

Ankle joint inflammation and nerve injury are associated with different Fkbp5 promoter DNA methylation landscape. A Adult male rats were injected with an inflammatory agent in the ankle joint or had spared nerve injury surgery on day 0 (N = 8/8/8/8). Both models induced significant mechanical hypersensitivity compared with their control groups, but there was no difference in the mechanical hypersensitivity between the two models (****P < 0.0001, ankle joint inflammation vs ankle joint inflammation control and nerve injury vs nerve injury control). B, C There was no significant change in Fkbp5 mRNA expression in the spinal cord and the hippocampus 30 days following inflammation and 30 days following nerve injury. mRNA levels were quantified by RTqPCR (N = 8/8). Data was normalised to control average. D We identified two CpG loci (cytosines at 8,059,052 & 8,059,072) with different levels of methylation between CFA and SNI tissue, in the brain and in the spinal cord, respectively (*P < 0.05)

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