Targeting miR-18a sensitizes chondrocytes to anticytokine therapy to prevent osteoarthritis progression.
Ontology highlight
ABSTRACT: Inflammation participates in the development of OA and targeting inflammatory signaling pathways is a potential strategy for OA treatment. IL-1β is one of the most important inflammatory factors to trigger the activation of NF-κB signaling and accelerate OA progression, whereas OA patients could hardly benefit from inhibiting IL-1β in clinic, suggesting the importance to further explore the details of OA inflammation. We here showed that expression of miR-18a in chondrocytes was specifically induced in response to IL-1β in vitro as well as in rat model of OA during which NF-κB signaling was involved, and that nuclear-translocated p65 directly upregulated miR-18a expression at transcriptional level. Further, increased miR-18a mediated hypertrophy of chondrocytes, resulting in OA degeneratio
SUBMITTER: Lian C
PROVIDER: S-EPMC7609664 | biostudies-literature | 2020 Nov
REPOSITORIES: biostudies-literature
ACCESS DATA