Publications
2016
Alsaleh G, Nehmar R, Blüml S, Schleiss C, Ostermann E, Dillenseger J P, Sayeh A, Choquet P, Dembele D, Francois A, Salmon J H, Paul N, Schabbauer G, Bierry G, Meyer A, Gottenberg J E, Haas G, Pfeffer S, Vallat L, Sibilia J, Bahram S, Georgel P
Reduced DICER1 expression bestows rheumatoid arthritis synoviocytes proinflammatory properties and resistance to apoptotic stimuli. Journal Article
In: Arthritis Rheumatol, vol. 68, no. 8, pp. 1839-1848, 2016, ISBN: 26882526.
Abstract | Links | BibTeX | Tags: DICER1 inflammation microRNA rheumatoid arthritis, PFEFFER, Unité ARN
@article{,
title = {Reduced DICER1 expression bestows rheumatoid arthritis synoviocytes proinflammatory properties and resistance to apoptotic stimuli.},
author = {G Alsaleh and R Nehmar and S Blüml and C Schleiss and E Ostermann and J P Dillenseger and A Sayeh and P Choquet and D Dembele and A Francois and J H Salmon and N Paul and G Schabbauer and G Bierry and A Meyer and J E Gottenberg and G Haas and S Pfeffer and L Vallat and J Sibilia and S Bahram and P Georgel},
url = {http://www.ncbi.nlm.nih.gov/pubmed/26882526},
doi = {10.1002/art.39641},
isbn = {26882526},
year = {2016},
date = {2016-01-01},
journal = {Arthritis Rheumatol},
volume = {68},
number = {8},
pages = {1839-1848},
abstract = {Objectives While the regulatory role of individual microRNAs in rheumatoid arthritis is well established, the role of DICER1 in the pathogenesis of the disease has not yet been investigated. Here, we analyze the expression of factors involved in miRNA biogenesis in synoviocytes (FLS) from RA patients and monitored arthritis triggered by K/BxN serum transfer in Dicer-deficient mice. Methods Genes and precursor miRNAs expression was quantified by RT-qPCR. miRNAs macroarray profiling was monitored by RT-qPCR. Cytokines were quantified by ELISA. Experimental arthritis in mice was achieved by serum transfer from K/BxN donors. Apoptosis was quantified using an ELISA assay. Results Here we report decreased DICER1 and mature miRNA expression in synovial fibroblasts isolated from rheumatoid arthritis (RA) patients. These cells are hyperresponsive to LPS, as evidenced by increased IL-6 secretion upon stimulation. Experimental serum transfer arthritis in Dicer mouse mutants confirmed that unbalanced miRNAs biogenesis correlates with enhanced inflammatory response. Finally, synoviocytes from both RA patients and from Dicer mutant mouse exhibit increased resistance to apoptotic stimuli. Conclusion Our work further substantiates the important role of DICER1 in the maintenance of homeostasis and the regulation of inflammatory responses. This article is protected by copyright. All rights reserved.},
keywords = {DICER1 inflammation microRNA rheumatoid arthritis, PFEFFER, Unité ARN},
pubstate = {published},
tppubtype = {article}
}
Objectives While the regulatory role of individual microRNAs in rheumatoid arthritis is well established, the role of DICER1 in the pathogenesis of the disease has not yet been investigated. Here, we analyze the expression of factors involved in miRNA biogenesis in synoviocytes (FLS) from RA patients and monitored arthritis triggered by K/BxN serum transfer in Dicer-deficient mice. Methods Genes and precursor miRNAs expression was quantified by RT-qPCR. miRNAs macroarray profiling was monitored by RT-qPCR. Cytokines were quantified by ELISA. Experimental arthritis in mice was achieved by serum transfer from K/BxN donors. Apoptosis was quantified using an ELISA assay. Results Here we report decreased DICER1 and mature miRNA expression in synovial fibroblasts isolated from rheumatoid arthritis (RA) patients. These cells are hyperresponsive to LPS, as evidenced by increased IL-6 secretion upon stimulation. Experimental serum transfer arthritis in Dicer mouse mutants confirmed that unbalanced miRNAs biogenesis correlates with enhanced inflammatory response. Finally, synoviocytes from both RA patients and from Dicer mutant mouse exhibit increased resistance to apoptotic stimuli. Conclusion Our work further substantiates the important role of DICER1 in the maintenance of homeostasis and the regulation of inflammatory responses. This article is protected by copyright. All rights reserved.