Proteins controlling catabolic and stress pathways are upregulated during total knee arthroplasty

Abstract

BACKGROUNDSkeletal muscle atrophy is common following total knee arthroscopy (TKA). A tourniquet is routinely used during TKA to create a bloodless field. Subsequent ischemia‐reperfusion (I/R) within muscle cells and tissue beds may activate cellular catabolic and stress pathways. We hypothesized that I/R increases gene expression and signaling proteins involved in muscle protein catabolism.PURPOSETo measure changes in transcripts and proteins involved in catabolic and stress pathways in older subjects undergoing TKA.METHODSSubjects between the ages 60–80 were studied in the operating room during surgery. Muscle biopsies were obtained at baseline (after anesthesia, immediately prior to tourniquet inflation), during maximal ischemia (just prior to tourniquet deflation), and during reperfusion.RESULTSTotal protein for FOXO3a, MAFbx, MuRF1, p‐38 MAPKs, and JNK were elevated relative to baseline during ischemia and reperfusion (p≤0.05). MAFbx, MuRF1, p‐38alpha, and JNK mRNA expression were increased during ischemia and reperfusion relative to baseline (p≤0.05).CONCLUSIONThese preliminary results suggest that I/R injury in muscle cells activates catabolic and stress pathways at the transcriptional and translational level during TKA in older adults.Support: NIH/NICHD K01HD057332.