Myostatin induces tumor necrosis factor‐α expression in rheumatoid arthritis synovial fibroblasts through the PI3K–Akt signaling pathway

2018 ◽  
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pp. 9793-9801 ◽  
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Chen‐Ming Su ◽  
Sung‐Lin Hu ◽  
Yi Sun ◽  
Jin Zhao ◽  
Chengqian Dai ◽  
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2007 ◽  
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Michael J. Lee ◽  
Andrew S. Islam ◽  
Jacqueline L. Rohrer ◽  
Victor M. Goldberg ◽  
...  

2006 ◽  
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Chuanyu Li ◽  
Yuelong Liu ◽  
Wan Mei ◽  
Shaohua Yu ◽  
...  

2013 ◽  
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Matthias Brock ◽  
Renate E. Gay ◽  
Beat A. Michel ◽  
Steffen Gay ◽  
...  

2021 ◽  
Vol 19 ◽  
pp. 205873922110317
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Chenghong Ni ◽  
Shiyi Zeng ◽  
Chen Zhang ◽  
Kehan Lao ◽  
Jifeng Wang ◽  
...  

Objective The objective is to examine the effect of tumor necrosis factor α (TNFα) on apoptosis and proliferation of rheumatoid arthritis synovial fibroblasts (RASFs) and to elucidate the regulatory roles of Kruppel-like factor 4 (KLF4) in TNFα-induced RASF apoptosis. Methods Changes in cell proliferation were measured using an 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide (MTT) assay, and changes in cell apoptosis were detected by flow cytometry and Hoechst 33258 staining. Changes in the apoptosis-related protein caspase-3 and the apoptosis-related genes bcl-2/bax were measured by western blot and real-time PCR, respectively Results TNFα stimulation increased cell proliferation ( p < 0.05), decreased cell apoptosis ( p < 0.05), declined caspase-3 expression ( p < 0.05), and upregulated bcl-2/bax level ( p < 0.05) in RASFs. KLF4 gene silencing decreased cell proliferation ( p < 0.05), increased cell apoptosis ( p < 0.05), upregulated caspase-3 expression ( p < 0.05), and downregulated bcl-2/bax level ( p < 0.05) induced by TNFα in RASFs. Conclusions TNFα caused a decrease in RASF apoptosis, and KLF4 promoted resistance to TNFα-induced apoptosis and cell proliferation.


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