Nitric oxide inhibits autophagy in human chondrocytes: Comment on the article by Sasaki et al

Shen, Chao; Chen, Xiaodong; Yan, Jun

doi:10.1002/art.37730

Cited by 7 publications

(4 citation statements)

References 31 publications

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“…This implies an increased intensity of thermal stress and thus a greater scope for the activation of additional cell death mechanisms. Furthermore, NO is known to be a potent inhibitor of autophagy (46, 47), and the alleviation of bleaching when NO was scavenged implies a reduced role for this pathway in the responses of the organisms examined here.…”

Section: Discussionmentioning

confidence: 92%

Nitric oxide mediates coral bleaching through an apoptotic‐like cell death pathway: evidence from a model sea anemone‐dinoflagellate symbiosis

Hawkins¹,

Bradley²,

Davy³

2013

FASEB j.

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Coral bleaching (involving the loss of symbiotic algae from the cnidarian host) is a major threat to coral reefs and appears to be mediated at the cellular level by nitric oxide (NO). In this study, we examined the specific role of NO in bleaching using the sea anemone Aiptasia pulchella, a model system for the study of corals. Exposure of A. pulchella to high-temperature shock (26-33°C over <1 h) or an NO donor (S-nitrosoglutathione) resulted in significant increases in host caspase-like enzyme activity. These responses were reflected in the intensities of bleaching, which were significantly higher in heat- or NO-treated specimens than in controls maintained in seawater at 26°C. Notably, the inhibition of caspase-like activity prevented bleaching even in the presence of an NO donor or at elevated temperature. The additional use of an NO scavenger controlled for effects mediated by agents other than NO. We also exposed A. pulchella to a more ecologically relevant treatment (an increase from 26 to 33°C over 6-7 d). Again, host NO synthesis correlated with the activation of caspase-like enzyme activity. Therefore, we conclude that NO's involvement in cnidarian bleaching arises through the regulation of host apoptotic pathways.

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Section: Discussionmentioning

confidence: 92%

Nitric oxide mediates coral bleaching through an apoptotic‐like cell death pathway: evidence from a model sea anemone‐dinoflagellate symbiosis

Hawkins¹,

Bradley²,

Davy³

2013

FASEB j.

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“…The protein of treated chondrocytes was separated on SDS-PAGE and then transferred to a polyvinylidene difluoride membrane as our previous described 22 . The membranes were blocked with 5% BSA followed by immunoblotting with LC3 (1:3000, Abcam, UK), Beclin-1 (1:300, Abcam, UK), p-Akt (1:500, Abcam, UK), p-P70S6K (1:250, Abcam, UK) and GAPDH (1:2500, Abcam, UK) antibodies overnight at 4 C and horseradish peroxidase-conjugated secondary antibodies were incubated for an hours at room temperature.…”

Section: Western Blotting Analysismentioning

confidence: 99%

Autophagy protects chondrocytes from glucocorticoids-induced apoptosis via ROS/Akt/FOXO3 signaling

Shen¹,

Cai²,

Peng³

et al. 2015

Osteoarthritis and Cartilage

113

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“…The sequence data reported in this paper have been deposited in the Gene Expression Omnibus (GEO) database with an accession no. GSE234821 ( 74 ). All other data are included in the article and/or SI Appendix .…”

Section: Data Materials and Software Availabilitymentioning

confidence: 99%

NOS inhibition reverses TLR2-induced chondrocyte dysfunction and attenuates age-related osteoarthritis

Shen

Serve

et al. 2023

Proc. Natl. Acad. Sci. U.S.A.

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Osteoarthritis (OA) is a joint disease featuring cartilage breakdown and chronic pain. Although age and joint trauma are prominently associated with OA occurrence, the trigger and signaling pathways propagating their pathogenic aspects are ill defined. Following long-term catabolic activity and traumatic cartilage breakdown, debris accumulates and can trigger Toll-like receptors (TLRs). Here we show that TLR2 stimulation suppressed the expression of matrix proteins and induced an inflammatory phenotype in human chondrocytes. Further, TLR2 stimulation impaired chondrocyte mitochondrial function, resulting in severely reduced adenosine triphosphate (ATP) production. RNA-sequencing analysis revealed that TLR2 stimulation upregulated nitric oxide synthase 2 ( NOS2 ) expression and downregulated mitochondria function-associated genes. NOS inhibition partially restored the expression of these genes, and rescued mitochondrial function and ATP production. Correspondingly, Nos2 −/− mice were protected from age-related OA development. Taken together, the TLR2–NOS axis promotes human chondrocyte dysfunction and murine OA development, and targeted interventions may provide therapeutic and preventive approaches in OA.

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Nitric oxide inhibits autophagy in human chondrocytes: Comment on the article by Sasaki et al

Cited by 7 publications

References 31 publications

Nitric oxide mediates coral bleaching through an apoptotic‐like cell death pathway: evidence from a model sea anemone‐dinoflagellate symbiosis

Nitric oxide mediates coral bleaching through an apoptotic‐like cell death pathway: evidence from a model sea anemone‐dinoflagellate symbiosis

Autophagy protects chondrocytes from glucocorticoids-induced apoptosis via ROS/Akt/FOXO3 signaling

NOS inhibition reverses TLR2-induced chondrocyte dysfunction and attenuates age-related osteoarthritis

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