Retinoid interferon-induced mortality19 (GRIM19) inhibits proliferation and invasion in rheumatoid arthritis fibroblast-like synoviocytes
Authors: Zhihui Wang
Dongkai Zhao
Zhiyu Jiang
Jinliang Gao
Journal: Biomedicine & Pharmacotherapy (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Apoptosis; GRIM19; Proliferation; Rheumatoid arthritis; STAT3.
Affiliations: Department of Rheumatology, the Affiliated Hospital, Changchun University of Chinese Medicine, Changchun, 130117, China., Department of Rheumatology, the Affiliated Hospital, Changchun University of Chinese Medicine, Changchun, 130117, China. Electronic address: .

Abstract:  Rheumatoid arthritis (RA) fibroblast-like synoviocytes (RA-FLS) are reportedly involved in RA initiation, progression, and perpetuation. Previously a study showed that retinoid interferon-induced mortality 19 (GRIM19) improved the clinical and histological features of collagen-induced arthritis (CIA),and also inhibited osteoclast formation. However, the role of GRIM19 in RA-FLS remains unclear. In this study, we explored the biological function and underlying mechanism of GRIM19 in cultured RA-FLS. The expression of GRIM19 in synovial tissues and RA-FLS was detected by real-time quantitative RT-PCR(qRT-PCR).The effects of GRIM19 on proliferation, migration, invasion, apoptosis, and inflammatory cytokines levels in RA-FLS were determined using CCK8, wound healing, transwell invasion, and flow cytometry assays, and enzyme-linked immunosorbent assay (ELISA), respectively.GRIM19 and its related protein expression levels were determined by western blot. We found that GRIM19expression was significantly decreased in synovial tissues and FLS from RA patients.GRIM19significantly inhibited proliferation, migration, and invasion; promoted apoptosis; and suppressed inflammatory cytokine secretion by RA-FLS. Moreover, GRIM19 overexpression significantly decreasedthe expression levels of signal transducer and activator of transcription 3(STAT3)and its downstreamproteins,CyclinD1, Bcl-2, and MMP-9. These data indicate that promoting the expression of GRIM19 may yield therapeutic benefits in the treatment of RA. 

Retracted: No

PubPeer comments:
 Two papers used the same flow-cytometry histograms to support their claims to have conducted (different) experiments. No authors in common. How did this happen? *[right]* Fig 2D.  Cell cycle arrest was measured in RA-FLS after the transfection of pCDNA3.1-GRIM19 and pCDNA3.1. *[left]* Fig 2F from [Hu et al (2018)] .  Flow cytometer detects cell arrest in SO-RB-50 cells transfected with si-NC or si-XIST. ![file] , 
 *[right]* Fig 6A.  STAT3, CyclinD1, Bcl-2 and MMP-9 protein expression were determined by western blot in RA-FLS after the transfection of pCDNA3.1-GRIM19 and pCDNA3.1. *[left]* Fig 5D from [Xia et al (2018)] .  The MMP-9 expression on ... protein levels were determined in A549 cells transfected with si-NC, si-HOXD-AS1, and si-HOXDAS1+miR-133b inhibitor . ![file] Protein blobs are repeated, in different orders. , 
 Potentially supporting the concern that this paper may have been outsourced to a third party, one image in Figure 4B seems to overlap with an image Figure 4B of another paper, DNA and Cell Biology (2016), doi: 10.1089 dna.2015.3171, discussed here: https: pubpeer.com publications 717BB701CF9D81B2CF74F636201C22. *** ![file] ,