Effect of SOD1K123R mutation on gene expression in nucleus pulposus cells treated with lactate.
Among musculoskeletal disorders, intervertebral disc degeneration (IVDD) is the primary cause of discogenic pain and associated disability and productivity loss in the workforce worldwide.Oxidative stress is an important inducing and aggravating factor of intervertebral disc degeneration. We found that lactate could induce the lactylation of SOD1 lysine 123 in nucleus pulposus cells, which impaired the antioxidant ability of the enzyme. Therefore, we mutated lysine (Lys) to arginine (Arg) at residue 123 of SOD1 in nucleus pulposus cells to eliminate the lactylation at residue 132 and investigated the underlying mechanism by RNA sequencing. Overall design: After knocking down SOD1 in nucleus pulposus cells, RNA-seq was performed after transfection of wild-type SOD1 and K123R mutant SOD1 with 10 mM lactate for 7 days