Endogenous adenosine maintains cartilage homeostasis and exogenous adenosine inhibits osteoarthritis progression

Carmen Corciulo, Matin Lendhey, Tuere Wilder, Hanna Schoen, Alexander Samuel Cornelissen, Gregory Chang, Oran D. Kennedy and Bruce N. Cronstein ()
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Carmen Corciulo: Department of Medicine-Division of Translational Medicine-NYU School of Medicine
Matin Lendhey: Department of Orthopedic Surgery-NYU School of Medicine
Tuere Wilder: Department of Medicine-Division of Translational Medicine-NYU School of Medicine
Hanna Schoen: Department of Medicine-Division of Translational Medicine-NYU School of Medicine
Alexander Samuel Cornelissen: Department of Medicine-Division of Translational Medicine-NYU School of Medicine
Gregory Chang: Department of Radiology-NYU School of Medicine
Oran D. Kennedy: Department of Orthopedic Surgery-NYU School of Medicine
Bruce N. Cronstein: Department of Medicine-Division of Translational Medicine-NYU School of Medicine

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract Osteoarthritis (OA) is characterized by cartilage destruction and chondrocytes have a central role in this process. With age and inflammation chondrocytes have reduced capacity to synthesize and maintain ATP, a molecule important for cartilage homeostasis. Here we show that concentrations of ATP and adenosine, its metabolite, fall after treatment of mouse chondrocytes and rat tibia explants with IL-1β, an inflammatory mediator thought to participate in OA pathogenesis. Mice lacking A2A adenosine receptor (A2AR) or ecto-5′nucleotidase (an enzyme that converts extracellular AMP to adenosine) develop spontaneous OA and chondrocytes lacking A2AR develop an ‘OA phenotype’ with increased expression of Mmp13 and Col10a1. Adenosine replacement by intra-articular injection of liposomal suspensions containing adenosine prevents development of OA in rats. These results support the hypothesis that maintaining extracellular adenosine levels is an important homeostatic mechanism, loss of which contributes to the development of OA; targeting adenosine A2A receptors might treat or prevent OA.

Date: 2017
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DOI: 10.1038/ncomms15019

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