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Chondrocyte-Specific Ablation of AMPKα1 Does Not Affect Bone Development or Pathogenesis of Osteoarthritis in Mice.

AMP-activated protein kinase (AMPK) acts as an intracellular sensor that modulates the energy balance within the cell. AMPKα1 is the dominant catalytic isoform expressed in the bone, but the significance of AMPKα1 in articular cartilage has not been well studied. In this study, we aimed to assess the in vivo function of AMPKα1 in chondrocytes. We created chondrocyte-specific AMPKα1 conditional knockout (KO) mice using Col2α1-Cre and analyzed and compared growth characteristics, HE staining, and AMPKα gene expression between wild-type (WT) mice and AMPKα1 conditional KO mice under normal physiological conditions or following activation of AMPK by metformin intake or treadmill exercise. Microcomputed tomography and safranin O-fast green staining were compared between WT and KO mice after induction of experimental osteoarthritis (OA). Our data showed that there was no somatic difference between WT mice and KO mice of the same age. Metformin intake and treadmill exercise did not alter the phenotype of KO mice, and no difference in cartilage degradation was observed in WT mice or in KO mice after induction of traumatic arthritis. We thought that chondrocyte-specific ablation of AMPKα1 had no effect on bone growth or on pathogenesis of OA in mice, probably because the feedback overexpression of AMPKα2 compensated for loss of AMPKα1 and maintained the combination of AMPKα subunits.