Richard F. Loeser, John A. Collins, Brian O. Diekman, Cathy S. Carlson

Research output: Contribution to journalLetterpeer-review

Original languageEnglish (US)
Pages (from-to)2162-2163
Number of pages2
JournalArthritis and Rheumatology
Issue number12
StatePublished - Dec 2020

Bibliographical note

Funding Information:
To the Editor: We appreciate the interest in our work expressed by Dr. Xu and Mr./Ms Huang. As they note, our study failed to demonstrate a protective effect of JNK1 or JNK2 deletion or combined deletion on the development of OA in the DM M mouse model. In addition, we noted more severe naturally occurring OA in aged mice with deletion of either JNK1 or JNK2 when compared with age-matched wild-type control mice. The more severe age-related OA in JNK-knockout mice was associated with increased expression of the cell senescence marker p16INK4a in the synovium and cartilage. Despite the negative findings we reported from our study, Dr. Xu and Mr./Ms Huang question whether JNK signaling might still be a valuable target to treat OA. They note conflicting results from previously published in vitro studies that demonstrated that JNK inhibition reduced catabolic and proinflammatory signaling, as well as findings from a prior study indicating that JNK2 deletion reduced cartilage damage in the DMM model.

PubMed: MeSH publication types

  • Letter
  • Research Support, N.I.H., Extramural
  • Comment

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