scholarly journals Correction: Oleuropein down-regulated IL-1β-induced inflammation and oxidative stress in human synovial fibroblast cell line SW982

2017 ◽  
Vol 8 (6) ◽  
pp. 2341-2341 ◽  
Author(s):  
Maria Luisa Castejón ◽  
Maria Ángeles Rosillo ◽  
Tatiana Montoya ◽  
Alejandro González-Benjumea ◽  
Jose G. Fernández-Bolaños ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Synovial Fibroblast ◽  
Fibroblast Cell ◽  
Fibroblast Cell Line ◽  
Human Synovial Fibroblast ◽  
And Oxidative Stress

Correction for ‘Oleuropein down-regulated IL-1β-induced inflammation and oxidative stress in human synovial fibroblast cell line SW982’ by Maria Luisa Castejón, et al., Food Funct., 2017, DOI: 10.1039/c7fo00210f.

Oleuropein down-regulated IL-1β-induced inflammation and oxidative stress in human synovial fibroblast cell line SW982

2017 ◽  
Vol 8 (5) ◽  
pp. 1890-1898 ◽  
Author(s):  
Maria Luisa Castejón ◽  
Maria Ángeles Rosillo ◽  
Tatiana Montoya ◽  
Alejandro González-Benjumea ◽  
Jose Maria Fernández-Bolaños ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Autoimmune Disease ◽  
Cell Line ◽  
Synovial Fibroblast ◽  
Fibroblast Cell ◽  
Synovial Fibroblasts ◽  
Fibroblast Cell Line ◽  
Inflammatory Autoimmune Disease ◽  
And Oxidative Stress

Rheumatoid arthritis (RA) is a chronic and systemic inflammatory autoimmune disease mainly characterized by aggressive hyperproliferation of synovial fibroblasts (SFs).

scholarly journals Small RNAs detected in exosomes derived from the MH7A synovial fibroblast cell line with TNF-α stimulation

PLoS ONE ◽  
2018 ◽  
Vol 13 (8) ◽  
pp. e0201851 ◽  
Author(s):  
Yosuke Takamura ◽  
Wataru Aoki ◽  
Atsushi Satomura ◽  
Seiji Shibasaki ◽  
Mitsuyoshi Ueda
Keyword(s):  
Cell Line ◽  
Small Rnas ◽  
Synovial Fibroblast ◽  
Fibroblast Cell ◽  
Fibroblast Cell Line ◽  
Tnf Α

scholarly journals Genomic Adaption and Mutational Patterns in a HaCaT Subline Resistant to Alkylating Agents and Ionizing Radiation

2021 ◽  
Vol 22 (3) ◽  
pp. 1146
Author(s):  
Reinhard Ullmann ◽  
Benjamin Valentin Becker ◽  
Simone Rothmiller ◽  
Annette Schmidt ◽  
Horst Thiermann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Copy Number ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Chromosomal Translocations ◽  
Dna Copy Number ◽  
Mutational Signatures ◽  
Copy Number Changes ◽  
And Oxidative Stress

Sulfur mustard (SM) is a chemical warfare agent that can damage DNA via alkylation and oxidative stress. Because of its genotoxicity, SM is cancerogenic and the progenitor of many chemotherapeutics. Previously, we developed an SM-resistant cell line via chronic exposure of the popular keratinocyte cell line HaCaT to increasing doses of SM over a period of 40 months. In this study, we compared the genomic landscape of the SM-resistant cell line HaCaT/SM to its sensitive parental line HaCaT in order to gain insights into genetic changes associated with continuous alkylation and oxidative stress. We established chromosome numbers by cytogenetics, analyzed DNA copy number changes by means of array Comparative Genomic Hybridization (array CGH), employed the genome-wide chromosome conformation capture technique Hi-C to detect chromosomal translocations, and derived mutational signatures by whole-genome sequencing. We observed that chronic SM exposure eliminated the initially prevailing hypotetraploid cell population in favor of a hyperdiploid one, which contrasts with previous observations that link polyploidization to increased tolerance and adaptability toward genotoxic stress. Furthermore, we observed an accumulation of chromosomal translocations, frequently flanked by DNA copy number changes, which indicates a high rate of DNA double-strand breaks and their misrepair. HaCaT/SM-specific single-nucleotide variants showed enrichment of C > A and T > A transversions and a lower rate of deaminated cytosines in the CpG dinucleotide context. Given the frequent use of HaCaT in toxicology, this study provides a valuable data source with respect to the original genotype of HaCaT and the mutational signatures associated with chronic alkylation and oxidative stress.

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