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IL6/sIL6R regulates TNF?-inflammatory response in synovial fibroblasts through modulation of transcriptional and post-transcriptional mechanisms.


ABSTRACT: INTRODUCTION:The clinical efficacy of specific interleukin-6 inhibitors has confirmed the central role of IL6 in rheumatoid arthritis (RA). However the local role of IL6, in particular in synovial fibroblasts (SF) as a direct cellular target to IL6/sIL6R signal is not well characterized. The purpose of the study was to characterize the crosstalk between TNF? and IL6/sIL6R signaling to the effector pro-inflammatory response of SF. METHODS:SF lines were stimulated with either TNF?, IL6/sIL6R, or both together, for the time and dose indicated for each experiment, and where indicated, cells were treated with inhibitors actinomycin D, adalimumab, ruxolitinib and cycloheximide. mRNA expression of cytokines, chemokines and matrix metalloproteases (MMPs) were analyzed by quantitative RT-PCR. Level of IL8/CXCL8 and CCL8 in culture supernatants was measured by ELISA. Mononuclear and polymorphonuclear cells migration assays were assessed by transwell using conditioned medium from SF cultures. Statistical analyses were performed as indicated in the corresponding figure legends and a p-value

SUBMITTER: Valin A 

PROVIDER: S-EPMC7596982 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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IL6/sIL6R regulates TNFα-inflammatory response in synovial fibroblasts through modulation of transcriptional and post-transcriptional mechanisms.

Valin Alvaro A   Del Rey Manuel J MJ   Municio Cristina C   Usategui Alicia A   Romero Marina M   Fernández-Felipe Jesús J   Cañete Juan D JD   Blanco Francisco J FJ   Ruano Yolanda Y   Criado Gabriel G   Pablos José L JL  

BMC molecular and cell biology 20201030 1


<h4>Introduction</h4>The clinical efficacy of specific interleukin-6 inhibitors has confirmed the central role of IL6 in rheumatoid arthritis (RA). However the local role of IL6, in particular in synovial fibroblasts (SF) as a direct cellular target to IL6/sIL6R signal is not well characterized. The purpose of the study was to characterize the crosstalk between TNFα and IL6/sIL6R signaling to the effector pro-inflammatory response of SF.<h4>Methods</h4>SF lines were stimulated with either TNFα,  ...[more]

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