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Osteoarthritis-Induced Metabolic Alterations of Human Hip Chondrocytes.

Authors:
Annett Eitner Simon Sparing Felix C Kohler Sylvia Müller Gunther O Hofmann Thomas Kamradt Hans-Georg Schaible Matthias Aurich

Biomedicines 2022 Jun 8;10(6). Epub 2022 Jun 8.

BG Trauma Center Bergmannstrost, 06112 Halle (Saale), Germany.

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, PGE 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.

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http://dx.doi.org/10.3390/biomedicines10061349DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9220245PMC
June 2022

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Osteoarthritis-Induced Metabolic Alterations of Human Hip Chondrocytes.

Authors:
Annett Eitner Simon Sparing Felix C Kohler Sylvia Müller Gunther O Hofmann Thomas Kamradt Hans-Georg Schaible Matthias Aurich

Biomedicines 2022 Jun 8;10(6). Epub 2022 Jun 8.

BG Trauma Center Bergmannstrost, 06112 Halle (Saale), Germany.

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. Read More

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Acta Histochem 2022 Apr 19;124(3):151867. Epub 2022 Feb 19.

Department of Anatomy, Research Block B, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India. Electronic address:

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Front Immunol 2021 27;12:722884. Epub 2021 Aug 27.

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