PUMA gene delivery to synoviocytes reduces inflammation and degeneration of arthritic joints

Saw-See Hong (), Hubert Marotte, Guillaume Courbon, Gary S. Firestein, Pierre Boulanger and Pierre Miossec ()
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Saw-See Hong: University of Lyon
Hubert Marotte: University Jean Monnet University of Lyon
Guillaume Courbon: University Jean Monnet University of Lyon
Gary S. Firestein: University of California at San Diego
Pierre Boulanger: University of Lyon
Pierre Miossec: University of Lyon

Nature Communications, 2017, vol. 8, issue 1, 1-12

Abstract: Abstract In rheumatoid arthritis (RA), the proliferation of fibroblast-like synoviocytes (FLS) is the cause of chronic inflammation in joints and of joint damage. Delivery of the pro-apoptotic gene PUMA to FLS via human adenovirus type 5 (HAdV5) vectors has been tested as a therapeutic approach, but efficiency is hampered by low transduction, as FLS do not express HAdV5 receptors on the cell surface. Here we show that efficient transduction of PUMA in FLS can be achieved by conjugating HAdV5 to a baculovirus, which binds to the cell surface via the envelope glycoprotein Gp64. Intra-articular injection in an adjuvant-induced rat model of RA induces apoptosis of FLS, leading to significant decrease in joint inflammation, joint damage, and bone loss with improvement in joint function and mobility. Our results demonstrate the therapeutic potential of PUMA gene therapy as a local treatment in various forms of arthritis in which abnormal FLS proliferation is implicated.

Date: 2017
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DOI: 10.1038/s41467-017-00142-1

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