LncRNA NKILA attenuates the progression of osteoarthritis through the targeted inhibition of the NF-κB pathway.

Background: Interleukin-1β (IL-1β) plays a crucial role in cartilage degeneration by inducing inflammatory cascades in chondrocytes, impairing their normal biological functions. Long non-coding RNA NKILA (lncRNA NKILA) has been implicated in osteoarthritis (OA), but its specific molecular mechanisms remain unclear. This study aims to elucidate the function and molecular regulatory mechanism of lncRNA NKILA in articular chondrocytes under IL-1β stimulation.
Methods: Primary human articular chondrocytes were cultured to investigate the effects of IL-1β on chondrocyte proliferation, apoptosis, and extracellular matrix metabolism. We employed Reverse Transcription Quantitative Polymerase Chain Reaction (RT-qPCR), western blot, flow cytometry, immunofluorescence, and nuclear mass separation assays to explore the interaction between lncRNA NKILA and the NFκB signaling pathway. Additionally, animal experiments were conducted to evaluate the therapeutic potential of modulating lncRNA NKILA expression in vivo.
Results: IL-1β treatment led to decreased chondrocyte proliferation and increased apoptosis. Our study demonstrated that IL-1β downregulates lncRNA NKILA, which weakens its inhibitory effect on the NFκB (Nuclear Factor Kappa B) signaling pathway. This downregulation results in increased NFκB activity and exacerbates chondrocyte degeneration. Notably, the upregulation of lncRNA NKILA significantly alleviated OA symptoms, indicating that NKILA could be a promising therapeutic target.
Conclusion: IL-1β reduces lncRNA NKILA expression, weakening its inhibition of NFκB signaling and promoting articular chondrocyte degeneration. Enhancing lncRNA NKILA expression offers a promising approach to mitigating OA, suggesting that NKILA could serve as a potential therapeutic target for OA treatment.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)