Version 1
: Received: 17 April 2023 / Approved: 17 April 2023 / Online: 17 April 2023 (09:38:19 CEST)
How to cite:
Hussein, N. J.; Alejo, A. L.; Prior, R.; Ball, H. C.; Safadi, F. F. TRAPPC9 Modulation Regulates IL-1β-Induced Chondrocyte Inflammation. Preprints2023, 2023040432. https://doi.org/10.20944/preprints202304.0432.v1
Hussein, N. J.; Alejo, A. L.; Prior, R.; Ball, H. C.; Safadi, F. F. TRAPPC9 Modulation Regulates IL-1β-Induced Chondrocyte Inflammation. Preprints 2023, 2023040432. https://doi.org/10.20944/preprints202304.0432.v1
Hussein, N. J.; Alejo, A. L.; Prior, R.; Ball, H. C.; Safadi, F. F. TRAPPC9 Modulation Regulates IL-1β-Induced Chondrocyte Inflammation. Preprints2023, 2023040432. https://doi.org/10.20944/preprints202304.0432.v1
APA Style
Hussein, N. J., Alejo, A. L., Prior, R., Ball, H. C., & Safadi, F. F. (2023). TRAPPC9 Modulation Regulates IL-1β-Induced Chondrocyte Inflammation. Preprints. https://doi.org/10.20944/preprints202304.0432.v1
Chicago/Turabian Style
Hussein, N. J., Hope C. Ball and Fayez F. Safadi. 2023 "TRAPPC9 Modulation Regulates IL-1β-Induced Chondrocyte Inflammation" Preprints. https://doi.org/10.20944/preprints202304.0432.v1
Abstract
Osteoarthritis (OA) is a debilitating degenerative joint disease that results in chronic pain and inflammation due to progressive mechanical and proteolytic cartilage degradation. Articular chondrocytes, the main cell type present in cartilage, are responsible for the deposition and maintenance of the cartilage extracellular matrix (ECM). However, following damage and inflammation, chondrocytes undergo hypertrophy, apoptosis, and contribute to inflammation and ECM degradation. NF-κB signaling is known to be dysregulated in OA. TRAPPC9, a vesicle trafficking protein, is known to directly activate NF-κB signaling in neuronal and bone cells, however, the biological significance of this protein in chondrocytes has yet to be elucidated. Here, we demonstrate that TRAPPC9 enhances pro-inflammatory gene and protein expression in murine primary articular chondrocytes. Furthermore, we show that TRAPPC9 elicits these responses via phosphorylation of P-100 that activates non-canonical NF-κB signaling. Taken together, these findings suggest TRAPPC9 may be a potential therapeutic target to decrease inflammation and matrix degradation during OA pathology.
Biology and Life Sciences, Cell and Developmental Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
