scholarly journals Neutrophil trafficking on-a-chip: an in vitro, organotypic model for investigating neutrophil priming, extravasation, and migration with spatiotemporal control

Lab on a Chip ◽  
2019 ◽  
Vol 19 (21) ◽  
pp. 3697-3705 ◽  
Author(s):  
Patrick H. McMinn ◽  
Laurel E. Hind ◽  
Anna Huttenlocher ◽  
David J. Beebe

Her we report a new microfluidic technology designed to facilitate the study of neutrophil trafficking and priming using primary human cells with a high degree of spatiotemporal control.

2019 ◽  
Author(s):  
Celia Lujan ◽  
Eleanor J. Tyler ◽  
Simone Ecker ◽  
Amy P. Webster ◽  
Eleanor R. Stead ◽  
...  

AbstractWe aim to improve anti-ageing drug discovery, currently achieved through laborious and lengthy longevity analysis. Recent studies demonstrated that the most accurate molecular method to measure human age is based on CpG methylation profiles, as exemplified by several epigenetics clocks that can accurately predict an individual’s age. Here, we developed CellAgeClock, a new epigenetic clock that measures subtle ageing changes in primary human cells in vitro. As such, it provides a unique tool to measure effects of relatively short pharmacological treatments on ageing. We validated the CellAgeClock against known longevity drugs such as rapamycin and trametinib. Moreover, we uncovered novel anti-ageing drugs, torin2 and Dactolisib (BEZ-235), demonstrating the value of our approach as a screening and discovery platform for anti-ageing strategies. The CellAgeClock outperforms other epigenetic clocks in measuring subtle ageing changes in primary human cells in culture. The tested drug treatments reduced senescence and other ageing markers, further consolidating our approach as a screening platform. Finally, we show that the novel anti-ageing drugs we uncovered in vitro, indeed increased longevity in vivo. Our method expands the scope of CpG methylation profiling from measuring human chronological and biological age from human samples in years, to accurately and rapidly detecting anti-ageing potential of drugs using human cells in vitro, providing a novel accelerated discovery platform to test sought after geroprotectors.


2019 ◽  
Vol 4 (1) ◽  
pp. e000217 ◽  
Author(s):  
Yoshimi Niwano ◽  
Atsuo Iwasawa ◽  
Kazuo Tsubota ◽  
Masahiko Ayaki ◽  
Kazuno Negishi

ObjectiveBlue light hazards for retina and ocular surface have been repeatedly described and many protective methods are introduced for retina; however, no study has been conducted on ocular surface protection. The purpose of this in vitro study was to examine phototoxicity and shade protection after blue light irradiation in primary human cells of corneal surface origin.Methods and analysisPrimary human cells of corneal surface origin were obtained from eye bank eyes. After blue light irradiation (405 nm) of these cells for 3 min, and a further 24 hours’ incubation, surviving viable cells were assessed by the methyl thiazolyl tetrazolium assay. Simultaneously, cell viability was determined in wells covered by ultraviolet and blue light shades.ResultsUnder subconfluent conditions, viable cells decreased by around 50% after blue light irradiation, compared with control cells without irradiation. The blue light phototoxicity was not blocked by the control shade, but the ultraviolet-blocking and blue light-blocking shades protected the cells from phototoxicity, producing a 30%–40% reduction (ultraviolet) and 15%–30% reduction (blue light) in viable cells.ConclusionThese results indicate that blue light injures ocular surface cells and the cells are protected from damage by a shade. We recommend blue light protection to maintain ocular health, especially in high-risk populations, such as people with dry eye, contact lens users, the malnourished and the elderly.


2019 ◽  
Vol 235 ◽  
pp. 415-423 ◽  
Author(s):  
Amy M. Zimmermann-Klemd ◽  
Viktoria Konradi ◽  
Carmen Steinborn ◽  
Annekathrin Ücker ◽  
Chiara Madlen Falanga ◽  
...  

2020 ◽  
pp. 1-20
Author(s):  
Rachel Verdon ◽  
Suzanne L. Gillies ◽  
David M. Brown ◽  
Theodore Henry ◽  
Lang Tran ◽  
...  

Mutagenesis ◽  
1996 ◽  
Vol 11 (4) ◽  
pp. 307-313 ◽  
Author(s):  
M. Kirsch-Volders ◽  
I. Tallon ◽  
C. Tanzarella ◽  
A. Sgura ◽  
T. Hermine ◽  
...  

2020 ◽  
Author(s):  
Bai Ji ◽  
Hongqiao Cai ◽  
Yan Jiao ◽  
Yahui Liu

Abstract Background: Liver cancer is one of the malignant tumors with the highest incidence in the world. Trophinin-associated protein (TROAP) was related with prognosis in liver cancer. However, the core genes associated with TROAP have not been identified yet. Methods: In this study, we performed in vitro cell experiments and bioinformatics analysis including screening of differentially expressed genes (DEGs), gene ontology (GO) enrichment analysis, and Kyoto Encyclopedia of Gene and Genome (KEGG) enrichment analysis. Hub genes with high degree of connectivity was picked out by establishing protein-protein interaction (PPI) network. Results: Our in vitro cell experiments suggested that down regulation of TROAP inhibited the proliferation and migration of liver cancer cells. A total of 20530 genes were analyzed and 953 differential expressed genes including 529 up-regulated DEGs and 424 down-regulated DEGs were detected. 10 hub genes with higher degree of connectivity including BUB1B, TOP2A, KIF23, UBE2C, KIF15, CDC20, PLK1, HJURP, BUB1, and DLGAP5 were selected. Conclusions: Our study may provide some evidence for the future genomic individualized treatment of liver cancer.


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