Evidence map›Paper›PMID 24468888›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2014

Activated macrophage-like synoviocytes are resistant to endoplasmic reticulum stress-induced apoptosis in antigen-induced arthritis.

Li-Jie Feng, Tong-Cui Jiang, Cheng-Yue Zhou, Chang-Liang Yu, Yu-Jun Shen, Jun Li, Yu-Xian Shen

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 22 citations in OpenAlex.

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  14. Endoplasmic reticulum stress is the crossroads of autophagy, inflammation, and apoptosis signaling pathways and participates in liver fibrosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Li-Jie FengSchool of Basic Medical Science, Anhui Medical University, 69 Meishan Road, 230032, Hefei, China.
Tong-Cui Jiang
Cheng-Yue Zhou
Chang-Liang Yu
Yu-Jun Shen
Jun Li
Yu-Xian Shen
Anhui Medical University · CNFirst Affiliated Hospital of Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo explore the characteristic expression of endoplasmic reticulum (ER) stress protein in antigen-induced arthritis models and the role of ER stress in arthritis.

methodsEffective animal models of rheumatoid arthritis in rabbits and rats were induced by methylated bovine serum albumin and Freund's complete adjuvant. Pathological changes were assessed by magnetic resonance imaging and histological analysis. The expression and localization of ER stress proteins in synovium and peritoneal macrophages (PMΦ) were analyzed by double immunofluorescence staining. RT-PCR was performed to detect mRNA expression of ER stress-related genes. Tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) levels in synoviocytes were measured by RT-PCR and radioimmunoassay.

resultsWe found that the ER stress marker BiP was highly up-regulated in arthritis synovium and extensively expressed in fibroblast-like synoviocytes (FLS) and macrophage-like synoviocytes (MLS). The expression of the pro-apoptotic factor CHOP/GADD153 was slightly elevated in inflammatory synovium and mainly localized in FLS, but insignificant in MLS. Unexpectedly, increased expression of CHOP was observed in PMΦ in arthritis rats. Likewise, cleaved caspase-3 was rarely expressed in MLS. In addition, induction of ER stress by tunicamycin resulted in significantly increased expression of pro-inflammatory molecules such as IL-1β and TNF-α in cultured inflammatory FLS.

conclusionDifferential activation of the ER stress proteins in synovium MLS may contribute to the resistance of synoviocytes to ER stress-induced apoptosis. Furthermore, ER stress is a potential mediator of arthritis inflammation.

Indexed as

ApoptosisEndoplasmic Reticulum StressActinsAnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticArthritis, ExperimentalCaspase 3CD68 MoleculeCells, CulturedFemaleInterleukin-1betaMacrophage ActivationMacrophagesMagnetic Resonance ImagingMaleActa2 protein, ratActinsAntigens, CDAntigens, Differentiation, MyelomonocyticCaspase 3CD68 antigen, humanCD68 MoleculeInterleukin-1betaTranscription Factor CHOPTumor Necrosis Factor-alpha

Identifiers

PMID24468888
OpenAlexW1991247547

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.