Fig 1: A proposed model depicting the dysregulation of polyamine (PA) metabolism in regulating human IDD. PAOX promotes the catabolism of PA and produces H2O2 as a source of reactive oxygen species (ROS) to cause oxidative stress and the resulting DAN damage, which accelerates the NP cell senescence and IDD progress. Spermidine and N-acetylcysteine (NAC) supplementation or cellular p16 clearance balance the PA metabolism in the disc and delay the IDD progress (figure is created in http://BioRender.com).
Fig 2: PAs and PAOX expression in NP cells from human intervertebral discs of different degeneration degrees. Representative images of (a) MRI of the disc from patients that yellow arrows refer to the collected segment; (b) safranin O and Masson staining of the NP tissue; (c) total PA concentration in NP tissue (n = 6); (d) immunohistochemical staining of PAOX in NP cells and the (e) quantification of positive cell ratio (n = 6). (f) Western blotting and measured by densitometry analyses and expressed as folds relative to grade 1 (n = 3). Data are presented as mean ± SD; **p < 0.01 and ***p < 0.001 compared to G1; #p < 0.05 and ###p < 0.001 compared to G3.
Fig 3: PPI network of oxidative stress-related genes (large spheres on the left) and ECM-related genes (small spheres on the right). We speculate the highlighted PAOX in the red dot-box and CDK2A have some interactions.
Supplier Page from Creative Biolabs for siRNA, Anti-PAOX, Unmodified