Abstract

Iron dysregulation is a known risk factor in the progression of osteoarthritis and is a feature of comorbid syndromes Alzheimer's disease, insulin resistance, and age‐related macular degeneration. Little, however, is known about iron homeostasis in healthy chondrocytes or whether iron dysregulation occurs in osteoarthritis. To gain information on this matter, we performed surgical destabilization of the medial meniscus on the right knee of 8‐week‐old mice. An untreated sham group served as the control. We found and document for the first time that chondrocytes produce hepcidin, and that both hepcidin and ferroportin expression is downregulated in osteoarthritic cartilage to a statistically significant extent. We found, however, that there was no statistically significant change in ferritin expression in osteoarthritic vs. healthy chondrocytes. We submit that this data, in conjunction with observed iron metabolism trends in other tissues, suggests a role for iron dysregulation in the pathogenesis of osteoarthritis.Support or Funding InformationOffice of Research and Creative Activities, Brigham Young UniversityThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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