X inactive-specific transcript regulates mitochondrial function and neuronal differentiation of stem cells via IGF2BP2/CPT1A axis in models of spinal cord injury

Figure 6 X inactive-specific transcript alleviated spinal cord injury by modulating neural stem cell differentiation via the insulin-like growth factor 2 mRNA binding protein 2/carnitine palmitoyl transferase 1A pathway. A: Relative RNA expression of X inactive-specific transcript (XIST) and carnitine palmitoyl transferase 1A on days 3 and 7 post-spinal cord injury (SCI), showing reduced expression in the SCI groups and elevated expression in the XIST day 7 group compared with the negative control (NC) day 7 group; B: Body weight measurements before surgery and 6 weeks after surgery, showing no significant differences in weight among the SCI, NC, and XIST groups; C: Basso Mouse Scale scores demonstrated a significant decline in the SCI group and a notable improvement in the XIST group compared with the NC group; D: ELISA measurement of inflammatory cytokine levels in spinal cord tissues, showing increased inflammation in the SCI model and reversal by XIST treatment. Data are presented as mean ± SD. ^aP < 0.05 indicates sham vs spinal cord injury (day 3 or 7), ^bP < 0.05 indicates spinal cord injury vs X inactive-specific transcript (day 7), ^cP < 0.05 indicates X inactive-specific transcript vs negative control (day 7). XIST: X inactive-specific transcript; NC: Negative control; CPT1A: Carnitine palmitoyl transferase 1A; SCI: Spinal cord injury; BMS: Basso Mouse Scale; IL: Interleukin; TNF: Tumor necrosis factor.