Figure 2From: Involvement of phosphatase and tensin homolog deleted from chromosome 10 in rodent model of neuropathic pain Changes in cellular specificity of endogenous PTEN in the dorsal horn of the spinal cord. (A) Western blots for phospho-PTEN, PTEN, and β-actin proteins from sham-operated and 14 days after CCI groups; (B) relative density of immunoblot of phospho-PTEN; (C) relative density of immunoblot of PTEN. Relative band intensities of phospho-PTEN and PTEN were quantified by densitometry and indicated as the percent change relative to that for the sham-operated group (100%). Western blotting of spinal dorsal horn tissue homogenate revealed that phospho-PTEN and PTEN protein expression was detectable in the sham-operated group, but CCI evoked upregulation of phospho-PTEN protein and downregulation of PTEN protein 14 days after CCI. Western blotting of β-actin was performed to verify the equivalent amounts of protein were loaded in each lane. Confocal double-immunofluorescent staining of PTEN (red) with NeuN (neuronal-specific marker; (D), green), GFAP (astrocyte specific marker; (E), green) OX-42 (microglial specific marker; (F), green) in the dorsal horn region of the lumbar spinal cord of sham-operated group. The merged images of (D), (E), and (F) (yellow; white arrow) indicate co-localization of PTEN with NeuN, GFAP, and OX-42 immunoreactive cells in the spinal cord, respectively. The confocal results showed that spinal PTEN was primarily co-localized with astrocytes. Scale bars are 50 μm for all images (D-F). Each bar in (B) and (C) represents the mean ± SEM with three rats per group. CCI-14 day: 14 days after CCI. *P < 0.05 compared with sham-operated group. CCI, chronic constriction injury; PTEN, phosphatase and tensin homolog deleted from chromosome 10; p-PTEN, phosphorylated PTEN.Back to article page