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  • Increase in NO causes osteoarthritis and chondrocyte apoptosis and chondrocyte ERK plays a protective role in the process

    Author(s)
    Chen, Qun
    Kao, Xibin
    Gao, Yan
    Chen, Jinghong
    Dong, Zhaoheng
    Chen, Chen
    Griffith University Author(s)
    Chen, Chen
    Year published
    2021
    Metadata
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    Abstract
    BACKGROUND: Nitric oxide (NO) and reactive oxygen species (ROS) play an important role in the pathology of human osteoarthritis (OA). Ankylosing spondylitis (AS) and atypical OA have similar clinical manifestations and often require differential diagnosis. The mechanism is however not totally clear yet. This study aims to investigate the effects of excessive NO-ROS in OA patients and the effects of extracellular signal-regulated kinases (ERK) pathway in NO-induced apoptosis of chondrocytes during OA progress. METHODS AND RESULTS: Serum samples from OA or AS as pathological control patients and healthy controls were collected ...
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    BACKGROUND: Nitric oxide (NO) and reactive oxygen species (ROS) play an important role in the pathology of human osteoarthritis (OA). Ankylosing spondylitis (AS) and atypical OA have similar clinical manifestations and often require differential diagnosis. The mechanism is however not totally clear yet. This study aims to investigate the effects of excessive NO-ROS in OA patients and the effects of extracellular signal-regulated kinases (ERK) pathway in NO-induced apoptosis of chondrocytes during OA progress. METHODS AND RESULTS: Serum samples from OA or AS as pathological control patients and healthy controls were collected for NO and related chemical measurements. The rabbit articular chondrocytes were cultured in vitro, and NO was applied by Sodium Nitroprusside (SNP) in culture medium to mimic OA condition in patients. The level of SNP-evoked chondrocyte apoptosis with or without PD98059 (ERK-specific inhibitor) was evaluated by TUNEL assay, Annexin V flow cytometry and Western blotting. The activity and mRNA expression of caspase-3 in chondrocytes were measured by assay kits and RT-PCR. The levels of NO and malondialdehyde (MDA) in serum were significantly higher in OA patients, while only MDA was significantly higher in AS patients. However, the level of superoxide dismutase (SOD) was lower in both OA and AS patients. SNP induced chondrocyte apoptosis was enhanced by PD98059 with increased protein expression and functional activity of caspase-3. CONCLUSIONS: The increase in nitric oxide occurs specifically in OA patients. ERK pathway may play a protective role on the NO-induced chondrocyte apoptosis, and inhibition of ERK pathway enhances the NO-induced apoptosis.
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    Journal Title
    Molecular Biology Reports
    DOI
    https://doi.org/10.1007/s11033-021-06731-0
    Note
    This publication has been entered as an advanced online version in Griffith Research Online.
    Subject
    Biochemistry and cell biology
    Apoptosis
    Caspase-3
    Chondrocytes
    Nitric oxide
    OA patients
    Publication URI
    http://hdl.handle.net/10072/409417
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