التفاصيل البيبلوغرافية
| العنوان: |
Osteoarthritis-Induced Metabolic Alterations of Human Hip Chondrocytes |
| المؤلفون: |
Annett Eitner, Simon Sparing, Felix C. Kohler, Sylvia Müller, Gunther O. Hofmann, Thomas Kamradt, Hans-Georg Schaible, Matthias Aurich |
| المصدر: |
Biomedicines, Vol 10, Iss 6, p 1349 (2022) |
| بيانات النشر: |
MDPI AG, 2022. |
| سنة النشر: |
2022 |
| المجموعة: |
LCC:Biology (General) |
| مصطلحات موضوعية: |
osteoarthritis, metabolic alterations, chondrocytes, oxygen consumption rate, mitochondrial ATP production, opioid peptides, Biology (General), QH301-705.5 |
| الوصف: |
Osteoarthritis (OA) alters chondrocyte metabolism and mitochondrial biology. We explored whether OA and non-OA chondrocytes show persistent differences in metabolism and mitochondrial function and different responsiveness to cytokines and cAMP modulators. Hip chondrocytes from patients with OA or femoral neck fracture (non-OA) were stimulated with IL-1β, TNF, forskolin and opioid peptides. Mediators released from chondrocytes were measured, and mitochondrial functions and glycolysis were determined (Seahorse Analyzer). Unstimulated OA chondrocytes exhibited significantly higher release of IL-6, PGE2 and MMP1 and lower production of glycosaminoglycan than non-OA chondrocytes. Oxygen consumption rates (OCR) and mitochondrial ATP production were comparable in unstimulated non-OA and OA chondrocytes, although the non-mitochondrial OCR was higher in OA chondrocytes. Compared to OA chondrocytes, non-OA chondrocytes showed stronger responses to IL-1β/TNF stimulation, consisting of a larger decrease in mitochondrial ATP production and larger increases in non-mitochondrial OCR and NO production. Enhancement of cAMP by forskolin prevented IL-1β-induced mitochondrial dysfunction in OA chondrocytes but not in non-OA chondrocytes. Endogenous opioids, present in OA joints, influenced neither cytokine-induced mitochondrial dysfunction nor NO upregulation. Glycolysis was not different in non-OA and OA chondrocytes, independent of stimulation. OA induces persistent metabolic alterations, but the results suggest upregulation of cellular mechanisms protecting mitochondrial function in OA. |
| نوع الوثيقة: |
article |
| وصف الملف: |
electronic resource |
| اللغة: |
English |
| تدمد: |
2227-9059 |
| Relation: |
https://www.mdpi.com/2227-9059/10/6/1349; https://doaj.org/toc/2227-9059 |
| DOI: |
10.3390/biomedicines10061349 |
| URL الوصول: |
https://doaj.org/article/475f46e04bd148fba25b1316ffd28765 |
| رقم الانضمام: |
edsdoj.475f46e04bd148fba25b1316ffd28765 |
| قاعدة البيانات: |
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