scholarly journals MiR-498 suppresses proliferation and inflammation in fibroblast-like synoviocytes in rheumatoid arthritis via targeting JAK1

2021 ◽  
Vol 18 (10) ◽  
pp. 2011-2017
Author(s):  
Lan Chai ◽  
Xian Zhen Zhang ◽  
Hai fang Ma ◽  
Fang Yuan
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Cycle ◽  
Polymerase Chain Reaction ◽  
Therapeutic Target ◽  
Cell Apoptosis ◽  
Inflammatory Responses ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Synovial Tissues ◽  
Fibroblast Like Synoviocytes

Purpose: To investigate the effect of microRNA 498 (miR-498) on proliferation and inflammation of rheumatoid arthritis (RA) fibroblast-like synoviocytes (RA-FLSs) in rheumatoid arthritis (RA). Methods: MiR-498 level was evaluated in both RA synovial tissues and RA-FLSs using real-time polymerase chain reaction (PCR). MicroRNA-498 overexpression or knockdown was performed in RAFLSs. Proliferation, apoptosis, cell cycle and inflammation induced by miR-498 mimics or inhibitor were used to explore the function of miR-498 in RA. Results: Expression level of miR-498 was downregulated in both RA synovial tissues and RA- FLSs. MicroRNA-498 mimics decreased proliferation and arrested cell cycle, whereas miR-498 inhibitor caused the opposite effects in RA-FLSs. In addition, miR-498 mimics suppressed inflammation and promoted cell apoptosis, while miR-498 inhibitor promoted inflammation and inhibited cell apoptosis in RA-FLSs. Furthermore, the effect of miR-498 on the proliferation, inflammation and apoptosis of RAFLSs was mediated by its ability to target and downregulate JAK1. Conclusion: These results indicate that miR-498 inhibits the proliferation and inflammatory responses of RA-FLSs by targeting JAK1, thus revealing a new therapeutic target for RA treatment.

scholarly journals miR-483-3p promotes IL-33 production from fibroblast-like synoviocytes by regulating ERK signaling in rheumatoid arthritis

2021 ◽  
Author(s):  
Kailin Zhang ◽  
Wenyi Fu ◽  
Shuai Zhao ◽  
Ting Jiao ◽  
Dan Wu ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Polymerase Chain Reaction ◽  
Protein Expression ◽  
Real Time ◽  
Signaling Pathway ◽  
Erk Signaling ◽  
Chain Reaction ◽  
Mrna And Protein Expression ◽  
Polymerase Chain ◽  
Fibroblast Like Synoviocytes

Abstract Our previous identified miR-483-3p to be highly expressed in synoviocytes from patients with rheumatoid arthritis (RA); however, its effects on inflammation of RA fibroblast-like synoviocytes (FLSs) have remained unclear. The expression of miR-483-3p and cytokines in RA FLSs was detected using quantitative real-time polymerase chain reaction. Enzyme-linked immunosorbent was conducted to determine interleukin (IL)-33 production from RA FLSs. Western blotting was employed to quantify the levels of p-ERK and total ERK. Overexpressed miR-483-3p significantly increased the mRNA and protein expression of IL-33, but not of IL-27 or IL-34, in RA FLSs, whereas miR-483-3p suppression showed the opposite effects. Furthermore, miR-483-3p upregulation activated the ERK signaling pathway. The ERK signaling inhibitor PD98059 partly reversed the elevation of IL-33 levels mediated by miR-483-3p overexpression. Our results reveal that miR-483-3p promotes IL-33 expression by regulating the ERK signaling pathway in RA FLSs. Thus, miR-483-3p may be a potential effective target for RA treatment.

Genistein and daidzein act on a panel of genes implicated in cell cycle and angiogenesis by Polymerase Chain Reaction arrays in human prostate cancer cell lines

2010 ◽  
Vol 34 (2) ◽  
pp. 200-206 ◽  
Author(s):  
Nadège Rabiau ◽  
Myriam Kossaï ◽  
Martin Braud ◽  
Nasséra Chalabi ◽  
Samir Satih ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Polymerase Chain Reaction ◽  
Cell Lines ◽  
Prostate Cancer Cell ◽  
Human Prostate Cancer ◽  
Chain Reaction ◽  
Human Prostate Cancer Cell ◽  
Prostate Cancer Cell Lines ◽  
Polymerase Chain

scholarly journals MicroRNA-425-5p modulates osteoporosis by targeting annexin A2

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Guanghua Chen ◽  
Guizhi Huang ◽  
Han Lin ◽  
Xinyou Wu ◽  
Xiaoyan Tan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bone Marrow ◽  
Cell Apoptosis ◽  
Chain Reaction ◽  
Potential Therapeutic Target ◽  
Treatment Of Osteoporosis ◽  
Qrt Pcr ◽  
Proliferation And Differentiation ◽  
Marrow Mesenchymal Stem Cells ◽  
Polymerase Chain

Abstract Background Studies have shown that the decrease of osteogenic differentiation of bone marrow mesenchymal stem cells (MSC) is an important mechanism of osteoporosis. The object of this study was to explore the role and mechanism of microRNA miR-425-5p in the differentiation of MSC. Methods The expression of miR-425-5p in MSC was detected by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Cell proliferation, cell cycle and apoptosis were detected by CCK-8 colorimetry and flow cytometry. The expression of TNF were detected by ELISA. Results Our data show that MiR-425-5p could modulate TNF-induced cell apoptosis, proliferation, and differentiation. ANXA2 is also the target of miR-425-5p and ANXA2 was involved in TNF-induced MSC cell apoptosis, proliferation, and differentiation. In addition, MiR-425-5p enhanced osteoporosis in mice. Conclusion MiR-425-5p might serve as a potential therapeutic target for the treatment of osteoporosis.

scholarly journals miR-431-5p regulates cell proliferation and apoptosis in fibroblast-like synoviocytes in rheumatoid arthritis by targeting XIAP

2020 ◽  
Author(s):  
Yuejiao Wang ◽  
Kailin Zhang ◽  
Xiaowei Yuan ◽  
Neili Xu ◽  
Shuai Zhao ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Real Time ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Proliferation And Apoptosis ◽  
Synovial Tissues ◽  
Proliferation Assays ◽  
Fibroblast Like Synoviocytes

Abstract Background miR-431-5p is dysregulated in various cancers and plays an important function in the development of cancer. However, its role in fibroblast-like synoviocytes (FLSs) in patients with rheumatoid arthritis (RA) remains to be understood.Methods Quantitative real-time polymerase chain reaction was used to detect the relative expression of miR-431-5p in synovial tissues and FLSs. Cell proliferation assays helped examine RA FLS proliferation. Flow cytometry was performed to determine apoptosis and cell cycle progression in RA FLSs. We used dual-luciferase assays to determine the correlation between miR-431-5p and its putative target, X-linked inhibitor of apoptosis (XIAP). Quantitative real-time PCR and western blotting were used to measure XIAP levels in synovial tissues and transfected RA FLSs.Results miR-431-5p was downregulated in synovial tissues and FLSs of patients with RA. Upregulation of miR-431-5p prohibited cell proliferation and the G0/G1-to-S phase transition, but promoted apoptosis in RA FLSs; while miR-431-5p inhibition showed the opposite results. miR-431-5p directly targeted XIAP in RA FLSs, and reversely correlated with XIAP levels in synovial tissues. Notably, XIAP silencing partially restored the effects of miR-431-5p inhibition in RA FLSs.Conclusion miR-431-5p regulates cell proliferation, apoptosis，and cell cycle of RA FLSs by targeting XIAP, suggesting its potential in the treatment of RA.

Polymerase chain reaction–based genotyping of the constant segment of immunoglobulin k shows weak or no association with rheumatoid arthritis

1995 ◽  
Vol 38 (10) ◽  
pp. 1526-1527 ◽  
Author(s):  
Rovinder Singh ◽  
Jinfeng Han ◽  
George Moxley
Keyword(s):  
Rheumatoid Arthritis ◽  
Polymerase Chain Reaction ◽  
Chain Reaction ◽  
Polymerase Chain

Epstein-Barr virus load in the peripheral blood of patients with rheumatoid arthritis: Accurate quantification using real-time polymerase chain reaction

2003 ◽  
Vol 48 (5) ◽  
pp. 1223-1228 ◽  
Author(s):  
Nathalie Balandraud ◽  
Jean Baptiste Meynard ◽  
Isabelle Auger ◽  
Helene Sovran ◽  
Benedicte Mugnier ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Polymerase Chain Reaction ◽  
Real Time ◽  
Peripheral Blood ◽  
Epstein Barr Virus ◽  
Chain Reaction ◽  
Barr Virus ◽  
Polymerase Chain ◽  
Epstein Barr ◽  
Accurate Quantification

scholarly journals The dual inhibitor of lipoxygenase and cyclooxygenase ML3000 decreases the expression of CXCR3 ligands

2007 ◽  
Vol 67 (4) ◽  
pp. 524-529 ◽  
Author(s):  
C Ospelt ◽  
M Kurowska-Stolarska ◽  
M Neidhart ◽  
B A Michel ◽  
R E Gay ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Polymerase Chain Reaction ◽  
Molecular Mechanisms ◽  
Synovial Fibroblasts ◽  
Target Cells ◽  
Chain Reaction ◽  
Dual Inhibitor ◽  
Protein Levels ◽  
Polymerase Chain ◽  
The Impact

Objective:To find previously unknown properties of ML3000, a competitive inhibitor of the cyclooxygenase and the lipoxygenase (LO) pathway.Methods:Gene expression of ML3000 treated and untreated rheumatoid arthritis synovial fibroblasts were measured with Affymetrix gene arrays. Downregulation of chemokine (C-X-C motif) ligands CXCL9, CXCL10 and CXCL11 was verified with Real-time polymerase chain reaction, CXCL10 protein levels were determined with ELISA. Rheumatoid arthritis synovial fibroblasts were treated with the cyclooxygenase inhibitor naproxen, the 5-LO inhibitor BWA4C and the 5-lipoxygenase-activating protein (FLAP) inhibitor MK886, and consecutive changes in CXCL10 protein levels measured. 5-LO expression was determined by polymerase chain reaction and Western blot.Results:In synovial fibroblasts and monocyte-derived macrophages ML3000 inhibited the tumour necrosis factor induced expression of CXCL9, CXCL10 and CXCL11, which are all ligands of the chemokine receptor CXCR3. No effect was observed in monocytes. Whereas inhibition of the cyclooxygenase pathway or the FLAP protein showed no effect, blockade of 5-LO significantly downregulated CXCL10 protein levels. 5-LO mRNA was detected in monocytes and in monocyte-derived macrophages. All tested cell types expressed 5-LO protein.Conclusions:ML3000 effectively downregulates CXCR3 ligands. This study confirms that a thorough analysis of the impact of a drug on its target cells cannot only reveal unexpected properties of a substance, but also helps to understand the underlying molecular mechanisms. Accordingly, our data provide the basis for further clinical studies testing the application of ML3000 in diseases such as rheumatoid arthritis or multiple sclerosis.

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