Effects of quercetin on apoptosis and extracellular matrix degradation of chondrocytes induced by oxidative stress‐mediated pyroptosis

2021 ◽  
Author(s):  
Qing Wang ◽  
Lujing Ying ◽  
Bing Wei ◽  
Yikui Ji ◽  
Yi Xu
Keyword(s):  
Oxidative Stress ◽  
Extracellular Matrix ◽  
Matrix Degradation ◽  
Extracellular Matrix Degradation

scholarly journals Bardoxolone-Methyl Prevents Oxidative Stress-Mediated Apoptosis and Extracellular Matrix Degradation in vitro and Alleviates Osteoarthritis in vivo

2021 ◽  
Vol Volume 15 ◽  
pp. 3735-3747
Author(s):  
Zhiying Pang ◽  
Zengxin Jiang ◽  
Runwen Zhu ◽  
Chunfeng Song ◽  
Han Tang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Extracellular Matrix ◽  
Matrix Degradation ◽  
Extracellular Matrix Degradation

Angiotensin II, oxidative stress, and extracellular matrix degradation during transition to LV failure in rats with hypertension

2006 ◽  
Vol 41 (6) ◽  
pp. 989-997 ◽  
Author(s):  
H TAKENAKA ◽  
Y KIHARA ◽  
Y IWANAGA ◽  
Y ONOZAWA ◽  
S TOYOKUNI ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Extracellular Matrix ◽  
Angiotensin Ii ◽  
Matrix Degradation ◽  
Extracellular Matrix Degradation

Cardamonin Alleviates Oxidative Stress, Cell Apoptosis Level and Extracellular Matrix Degradation by Inhibiting NF-kb in ILβ-1 -Induced Chondrocytes

2020 ◽  
Vol 10 (5) ◽  
pp. 589-595
Author(s):  
Chongxin Li ◽  
Wei Zeng
Keyword(s):  
Oxidative Stress ◽  
Extracellular Matrix ◽  
Cell Apoptosis ◽  
Cell Model ◽  
Joint Disease ◽  
Protective Effects ◽  
Matrix Degradation ◽  
Extracellular Matrix Degradation ◽  
Apoptosis Detection ◽  
Apoptosis Level

Currently, osteoarthritis as degenerative chronic joint disease remains unsolved and finding the effective targeting therapeutic agent is pressing. Therefore, in this research, we aimed to investigate the effects of cardamonin, the NF-kb inhibitor, in cell model of osteoarthritis. IL-1β that induced chondrocytes served as the cell model of osteoarthritis. The cells were divided into control, IL-1β and IL-1+ cardamonin groups. Western blot assays were performed for assessment of protein expression level and PCR for gene level. Flow cytometry was used for cell apoptosis detection. MDA, LDH SOD and ROS were detected by corresponding kits. The NF-kb was activated by IL-1. The entrance of NF-kb into cell nucleus was inhibited by cardamonin in IL-1β-induced cells. The MDA, LDH and ROS were increased by IL-1β and SOD was down-regulated by IL-1β. This effect of IL-1β was reduced by cardamonin. The cell apoptosis and pro-apoptosis proteins were increased and BCl-2 was down-regulated in IL-1β-induced cells. After cardamonin treatment, this effect was inhibited. The extracellular matrix degradation as well as the relative degradation enzymes was elevated by IL-1β, and this effect was further inhibited by cardamonin as well. Cardamonin exerted protective effects via alleviating oxidative stress, cell apoptosis level and extracellular matrix degradation by inhibiting NF-kb in IL-1β-induced chondrocytes. Cardamonin as NF-kb inhibitor was a promising drug for therapy of osteoarthritis.

scholarly journals Cytokines, Angiogenesis, and Extracellular Matrix Degradation are Augmented by Oxidative Stress in Endometriosis

2020 ◽  
Vol 40 (5) ◽  
pp. 390-397 ◽  
Author(s):  
Amalesh Nanda ◽  
Thangapandi K. ◽  
Priyanka Banerjee ◽  
Mainak Dutta ◽  
Tsering Wangdi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Extracellular Matrix ◽  
Matrix Degradation ◽  
Extracellular Matrix Degradation

Avicularin suppresses cartilage extracellular matrix degradation and inflammation via TRAF6/MAPK activation

Phytomedicine ◽  
2021 ◽  
pp. 153657
Author(s):  
Zi-ling Zou ◽  
Ming-hui Sun ◽  
Wei-feng Yin ◽  
Lei Yang ◽  
Ling-yi Kong
Keyword(s):  
Extracellular Matrix ◽  
Matrix Degradation ◽  
Mapk Activation ◽  
Extracellular Matrix Degradation ◽  
Cartilage Extracellular Matrix

Targeting TSP-1 decreased periodontitis by attenuating extracellular matrix degradation and alveolar bone destruction

2021 ◽  
Vol 96 ◽  
pp. 107618
Author(s):  
Xiaoxiao Liu ◽  
Juan Jin ◽  
Yajing Liu ◽  
Zhenguo Shen ◽  
Rongquan Zhao ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Alveolar Bone ◽  
Bone Destruction ◽  
Matrix Degradation ◽  
Extracellular Matrix Degradation

scholarly journals The phosphatase Shp1 interacts with and dephosphorylates cortactin to inhibit invadopodia function

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Alessia Varone ◽  
Chiara Amoruso ◽  
Marcello Monti ◽  
Manpreet Patheja ◽  
Adelaide Greco ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Tyrosine Phosphatase ◽  
Melanoma Cells ◽  
Matrix Degradation ◽  
Extracellular Matrix Degradation ◽  
Invadopodia Formation ◽  
Interference Rna

Abstract Background Invadopodia are actin-based cell-membrane protrusions associated with the extracellular matrix degradation accompanying cancer invasion. The elucidation of the molecular mechanisms leading to invadopodia formation and activity is central for the prevention of tumor spreading and growth. Protein tyrosine kinases such as Src are known to regulate invadopodia assembly, little is however known on the role of protein tyrosine phosphatases in this process. Among these enzymes, we have selected the tyrosine phosphatase Shp1 to investigate its potential role in invadopodia assembly, due to its involvement in cancer development. Methods Co-immunoprecipitation and immunofluorescence studies were employed to identify novel substrate/s of Shp1AQ controlling invadopodia activity. The phosphorylation level of cortactin, the Shp1 substrate identified in this study, was assessed by immunoprecipitation, in vitro phosphatase and western blot assays. Short interference RNA and a catalytically-dead mutant of Shp1 expressed in A375MM melanoma cells were used to evaluate the role of the specific Shp1-mediated dephosphorylation of cortactin. The anti-invasive proprieties of glycerophosphoinositol, that directly binds and regulates Shp1, were investigated by extracellular matrix degradation assays and in vivo mouse model of metastasis. Results The data show that Shp1 was recruited to invadopodia and promoted the dephosphorylation of cortactin at tyrosine 421, leading to an attenuated capacity of melanoma cancer cells to degrade the extracellular matrix. Controls included the use of short interference RNA and catalytically-dead mutant that prevented the dephosphorylation of cortactin and hence the decrease the extracellular matrix degradation by melanoma cells. In addition, the phosphoinositide metabolite glycerophosphoinositol facilitated the localization of Shp1 at invadopodia hence promoting cortactin dephosphorylation. This impaired invadopodia function and tumor dissemination both in vitro and in an in vivo model of melanomas. Conclusion The main finding here reported is that cortactin is a specific substrate of the tyrosine phosphatase Shp1 and that its phosphorylation/dephosphorylation affects invadopodia formation and, as a consequence, the ability of melanoma cells to invade the extracellular matrix. Shp1 can thus be considered as a regulator of melanoma cell invasiveness and a potential target for antimetastatic drugs.

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