Journal
ELIFE
Volume 11, Issue -, Pages -Publisher
eLIFE SCIENCES PUBL LTD
DOI: 10.7554/eLife.80725
Keywords
glutamine; metabolism; inflammation; chondrocyte; osteoarthritis; human; Mouse
Categories
Funding
- NIH/NIAMS [R01- AI161022]
- Shriners Hospital for Children
- NIH Core Center for Musculoskeletal Biology and Medicine
- [P30 AR074992]
- [R01- AR072623]
- [R01- AR076758]
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Osteoarthritis is a common joint disease with a prominent inflammatory component, while the role of glutamine metabolism in chondrocytes, especially in the context of inflammation, remains poorly understood. Studies show that mouse chondrocytes utilize glutamine for energy production and anabolic processes, and glutamine deprivation can lead to metabolic reprogramming and decreased inflammatory response.
Osteoarthritis is the most common joint disease in the world with significant societal consequences but lacks effective disease-modifying interventions. The pathophysiology consists of a prominent inflammatory component that can be targeted to prevent cartilage degradation and structural defects. Intracellular metabolism has emerged as a culprit of the inflammatory response in chondrocytes, with both processes co-regulating each other. The role of glutamine metabolism in chondrocytes, especially in the context of inflammation, lacks a thorough understanding and is the focus of this work. We display that mouse chondrocytes utilize glutamine for energy production and anabolic processes. Furthermore, we show that glutamine deprivation itself causes metabolic reprogramming and decreases the inflammatory response of chondrocytes through inhibition of NF-?B activity. Finally, we display that glutamine deprivation promotes autophagy and that ammonia is an inhibitor of autophagy. Overall, we identify a relationship between glutamine metabolism and inflammatory signaling and display the need for increased study of chondrocyte metabolic systems.
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