Rheumatoid Arthritis Fibroblast-like Synoviocyte Suppression Mediated by PTEN Involves Survivin Gene Silencing

Chen, Danna; Liu, Dongdong; Liú, Dan; He, Min; Peng, Anping; Xu, Jiaxi; Lin, Li; Luo, Fudong; Chen, Lin; Huang, Xianzhang; Zhang, Junhua; Xu, Jianhua

doi:10.1038/s41598-017-00517-w

Cited by 19 publications

(21 citation statements)

References 28 publications

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“…RA is a progressive and debilitating autoimmune disease (27). Synovial tissue is principally composed of fibroblast-like synovial cells, which are closely associated with the pathogenesis and development of RA, particularly joint damage (28).…”

Section: Discussionmentioning

confidence: 99%

Effect of astragalosides on long non-coding RNA expression profiles in rats with adjuvant-induced arthritis

Jiang

Liu

et al. 2019

Int J Mol Med

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Rheumatoid arthritis (RA) is an autoimmune disease of unknown etiology, which occurs in ~1.0% of the general population. Increasing studies have suggested that long non-coding RNAs (lncRNAs) may serve important roles in various biological processes and may be associated with the pathogenesis of different types of disease, including RA. Astragalosides (AST) has been used as a traditional Chinese medicine for the treatment of RA. However, the mechanism underlying its therapeutic effect has remained unclear to date. Thus, there is an urgent need to elucidate the possible mechanism of AST in the treatment of RA from the perspective of lncRNAs. In the present study, the lncRNAs and mRNAs of a vehicle group, animal model group and AST treatment (control) group were determined by Arraystar Rat lncRNA/mRNA microarray. The differentially expressed genes with a fold change >1.5 and P<0.05 were selected and analyzed. Gene Ontology (GO) and pathway analysis was performed using the Database for Annotation, Visualization and Integration Discovery, and the coding-non-coding gene co-expression network was drawn based on the correlation analysis between the differentially expressed lncRNAs and mRNAs. Based on node degree and the correlation between bioinformatics analysis and RA, the critical differentially expressed lncRNAs were selected, analyzed and verified by reverse transcription-quantitative PCR (RT-qPCR) analysis. The results showed that, following AST treatment, up to 75 lncRNAs and 247 mRNAs were found to be differentially expressed among the three groups. GO and pathway analysis manifested that 135 GO terms and 17 pathways were enriched by differentially expressed genes. Four lncRNAs (MRAK012530, MRAK132628, MRAK003448 and XR_006457) were selected as the critical lncRNAs and their trend in expression showed consistency between the RT-qPCR and microarray data. In conclusion, AST had a regulatory effect on differentially expressed lncRNAs during the development of RA, and four lncRNAs could be selected as critical therapeutic targets of AST.

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Section: Discussionmentioning

confidence: 99%

Effect of astragalosides on long non-coding RNA expression profiles in rats with adjuvant-induced arthritis

Jiang

Liu

et al. 2019

Int J Mol Med

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“…| 21579 study which showed that both the overexpression of PTEN, a negative regulator of survivin, and survivin knockdown simultaneously inhibit the migration of FLS and IL-6 production (D. Chen et al, 2017). The STAT3mediated survivin expression in the inflammatory condition is not limited to the IL-6, other cytokines, including IL-11 and IL-22, can also induce survivin production through PI3K/Akt pathway and STAT3 activation (Nguyen, Putoczki, & Ernst, 2015).…”

Section: Influence Of Survivin Expression On Inflammatory Reactions In Ramentioning

confidence: 99%

Survivin a pivotal antiapoptotic protein in rheumatoid arthritis

Zafari

Rafiei

Esmaeili

et al. 2019

Journal Cellular Physiology

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Rheumatoid arthritis (RA) is an autoimmune disease, pathologically characterized by lymphocyte infiltration of the synovial membrane that leads to chronic inflammation and progressive joint damage. RA develops as a result of increased cell infiltration and cell proliferation as well as impaired cell death. Activated cells in joints including lymphocytes and fibroblast-like synoviocytes (FLS) survive for a long time as a consequence of compromised apoptosis, but the mechanism underlying cell survival in synovium remains to be firmly established. Inhibition of apoptosis by survivin, as a critical antiapoptotic protein, contributes to both the persistence of autoreactive T lymphocytes and tumor-like phenotype of FLS in RA. In addition to the antiapoptotic role, survivin also has prognostic relevance in RA prodromal phase. Hence, this review provides an overview of the current knowledge regarding the involvement of survivin protein in the pathogenesis of RA.

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“…The blocking of the following signal transducer and activator of transcription 3 (STAT3) signaling pathway leading to the induction of apoptosis and consequently, the level of survivin expression decreases (Aoki, Feldman, & Tosato, 2003). The regulation network of survivin is involved in the phosphoinositide 3-kinase (PI3K) and Akt pathways which is illustrated in Figure 2 (Chen et al, 2017). Suppression of RA-FLS-mediated by PTEN gene is also participated in survivin silencing (Chen et al, 2017) (Jackson & Bartek, 2009).…”

Section: Activation Of Immune Signaling By Survivinmentioning

confidence: 99%

“…The regulation network of survivin is involved in the phosphoinositide 3-kinase (PI3K) and Akt pathways which is illustrated in Figure 2 (Chen et al, 2017). Suppression of RA-FLS-mediated by PTEN gene is also participated in survivin silencing (Chen et al, 2017) (Jackson & Bartek, 2009). Researchers indicated that DNA damage sensors play a key role in the recognition of foreign DNA aberrantly located in the cytoplasm to activate immune signaling.…”

Section: Activation Of Immune Signaling By Survivinmentioning

confidence: 99%

Survivin modulatory role in autoimmune and autoinflammatory diseases

Pahlavan

Kahroba

Samadi

et al. 2019

Journal Cellular Physiology

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Baculoviral IAP repeat containing 5 (BIRC5) gene encodes the important protein as survivin, a multifunctional protein, which is involved in cellular and molecular networks, progression of cell cycle, homeostasis, developmental morphogenesis, and apoptosis. The proximal BIRC5 promoter possesses specific binding sites for key transcription factors such as nuclear factor κB and signal transducer and activator of transcription 3. Upregulation of survivin exacerbates the autoimmune diseases (AIDs) including multiple sclerosis and myasthenia gravis by reducing the activity threshold of survivin-specific cytotoxic T cells. DNA damage along with upregulation or downregulation of survivin have been demonstrated in initiation and pathogenesis of cancers and AIDs. However, detailed mechanism of survivin function in pathogenesis of AIDs is not well understood. This review focuses on the structure, specificity, regulation, and function of survivin in physiologic conditions and pathogenesis of AIDs.

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Rheumatoid Arthritis Fibroblast-like Synoviocyte Suppression Mediated by PTEN Involves Survivin Gene Silencing

Cited by 19 publications

References 28 publications

Effect of astragalosides on long non-coding RNA expression profiles in rats with adjuvant-induced arthritis

Effect of astragalosides on long non-coding RNA expression profiles in rats with adjuvant-induced arthritis

Survivin a pivotal antiapoptotic protein in rheumatoid arthritis

Survivin modulatory role in autoimmune and autoinflammatory diseases

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