miR‑155‑5p regulates macrophage M1 polarization and apoptosis in the synovial fluid of patients with knee osteoarthritis

Li, Gui-Shi; Cui, Lei; Wang, Guangda

doi:10.3892/etm.2020.9500

Cited by 18 publications

(15 citation statements)

References 32 publications

(39 reference statements)

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“…miR-155-5p can serve as the potential therapeutic target for KOA [ 6 ]. Our results demonstrated significantly upregulated miR-155 expression in LPS-induced chondrocytes.…”

Section: Discussionmentioning

confidence: 99%

“…A relevant study demonstrated indirect evidence of the role of chronic inflammation in patients with rheumatoid arthritis in metabolic syndrome and atherosclerosis development [ 5 ]. A variety of pro-inflammatory cytokines including interleukin 1 beta (IL-1β) and IL-18 secreted by an increased number of inflammatory cells exacerbate OA [ 6 , 7 ]. KOA affects 3 compartments of knee joints (patellofemoral, medial, and lateral joint), which usually slowly develops over 10–15 years and interferes with the daily life activities [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

“…Studying the role of miRNAs in joint physiology and pathology may provide reference for the diagnosis, prevention, and treatment of OA [ 15 ]. miRNAs are small, single-stranded RNAs, which are related to a variety of diseases, such as cancer, OA and diabetes [ 6 , 16 ]. miR-155 is reported to be upregulated in lipopolysaccharide (LPS)-induced inflammatory articular chondrocyte [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

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miR-155 inhibits chondrocyte pyroptosis in knee osteoarthritis by targeting SMAD2 and inhibiting the NLRP3/Caspase-1 pathway

Xiu

Li³

et al. 2022

J Orthop Surg Res

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Objective Knee osteoarthritis (KOA) is based on degenerative pathological changes. miR-155 is involved in regulating KOA. This study estimated the mechanism of miR-155 in mouse KOA chondrocytes. Methods Mouse KOA chondrocyte model was established by lipopolysaccharide (LPS) induction and identified through Collagen II immunofluorescence staining and toluidine blue staining. LPS-induced KOA chondrocytes were transfected with miR-155 inhibitor or/and si-SMAD2, followed by the evaluation of miR-155 expression, pyroptosis, the SMAD2/NLRP3/Caspase-1 axis-related protein levels, IL-1β and 1L-18 levels, and cell viability by RT-qPCR, FAM-FLICA Caspase-1 Detection Kit, Western blot, ELISA, and MTT assays, respectively. The binding sites between miR-155 and SMAD2 were predicted online and the binding relationship was verified by dual-luciferase assay. Results miR-155 was highly-expressed in LPS-induced KOA chondrocytes. miR-155 knockdown increased cell viability and decreased pyroptotic chondrocytes, and Caspase-1, 1L-1β and 1L-18 levels. miR-155 targeted SMAD2. SMAD2 knockdown partially annulled the effects of miR-155 silencing on inhibiting KOA chondrocyte pyroptosis. NLRP3 pathway was activated in LPS-induced KOA chondrocytes, inhibited after miR-155 knockdown, and activated again after further SMAD2 knockdown. NLRP3 inhibition suppressed Caspase-1, IL-1β, and IL-18 levels and chondrocyte pyroptosis and increased cell viability. Conclusion miR-155 knockdown inhibited the NLRP3/Caspase-1 pathway by targeting SMAD2, thus inhibiting mouse KOA chondrocyte pyroptosis.

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“…miR-155-5p can serve as the potential therapeutic target for KOA [ 6 ]. Our results demonstrated significantly upregulated miR-155 expression in LPS-induced chondrocytes.…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

miR-155 inhibits chondrocyte pyroptosis in knee osteoarthritis by targeting SMAD2 and inhibiting the NLRP3/Caspase-1 pathway

Xiu

Li³

et al. 2022

J Orthop Surg Res

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“…miR155 is overexpressed and plays a key role in the pathophysiology of inflammatory diseases including autoimmune arthritis, osteoarthritis, periodontitis (11, 22, 53). An elevated level of miR155 in arthritis promotes M1 macrophage polarization and inflammation (53). Prevention of bone loss in inflammatory diseases using currently available therapeutic approaches is not satisfactory.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-155 regulates osteogenesis and bone mass phenotype via targeting S1PR1 gene

Zheng

et al. 2022

Preprint

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MicroRNA-155 (miR155) is overexpressed in various inflammatory diseases and cancer, in which bone resorption and osteolysis are frequently observed. However, the role of miR155 on osteogenesis and bone mass phenotype is still unknown. Here, we report a low bone mass phenotype in the long bone of miR155-Tg mice compared with control mice. In contrast, miR155-KO mice showed a high bone mass phenotype. miR155-KO mice showed robust bone regeneration in the ectopic and orthotopic model, but miR155-Tg mice showed compromised bone regeneration compared with the control mice. Similarly, the osteogenic differentiation potential of bone marrow stromal stem cells (BMSCs) from miR155-KO mice was robust and miR155-Tg was compromised compared with that of control mice. Moreover, miR155 knockdown in BMSCs from control mice showed higher osteogenic differentiation potential, supporting the results from miR155-KO mice. TargetScan analysis predicted S1PR1 as a target gene of miR155, which was further confirmed by luciferase assay and miR155 knockdown. S1PR1 overexpression in BMSCs robustly promoted osteogenic differentiation without affecting cell viability and proliferation. Thus, miR155 showed a catabolic effect on osteogenesis and bone mass phenotype via interaction with the S1PR1 gene, suggesting inhibition of miR155 as a potential strategy for bone regeneration and bone defect healing.

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“…A�� l� ��l�� c�ll �� c�� l� ��l�� l��, �� of various processes (30,31). As the most common chronic joint disease in the elderly population, OA is characterized by the progressive destruction of articular cartilage (32,33). Previous �� c�� c��c�� c��l�� with the severity of OA (34,35).…”

Section: Discussionmentioning

confidence: 99%

Reduced miR‑519d‑3p levels in the synovium and synovial fluid facilitate the progression of post‑traumatic osteoarthritis by targeting VEGF

Gao

Xia

2021

Exp Ther Med

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T�� T�� sion and clinical significance of miR-519d-3p in patients with post-traumatic osteoarthritis (PTOA). The levels of miR-519d-3p in the synovium and synovial fluid (SF) of all subjects were detected by reverse transcription-quantitative polymerase chain reaction. The results of the present study demonstrated that the levels of miR-519d-3p in the synovium and SF of patients with PTOA were significantly lower, but that the VEGF content was significantly higher, compared with that of control group. Dual-luciferase reporter and Western blot assays demonstrated that VEGF was a target gene of miR-519d-3p. Furthermore, miR-519d-3p inhibitor-induced cell apoptosis, and cell cycle arrest could be partially reversed by silencing VEGF. Additionally, the level of miR-519d-3p in the synovium and SF of patients with PTOA was negatively correlated with the level of VEGF. ROC analysis demonstrated that miR-519d-3p levels in the synovium and SF could effectively differentiate patients with PTOA from healthy controls, with areas under the ROC curve of 0.928 and 0.896, respectively. In conclusion, reduction of miR-519d-3p in the synovium and SF resulted in the upregu� lation of VEGF in patients with PTOA, and miR-519d-3p may be a potential therapeutic target of PTOA.

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miR‑155‑5p regulates macrophage M1 polarization and apoptosis in the synovial fluid of patients with knee osteoarthritis

Cited by 18 publications

References 32 publications

miR-155 inhibits chondrocyte pyroptosis in knee osteoarthritis by targeting SMAD2 and inhibiting the NLRP3/Caspase-1 pathway

miR-155 inhibits chondrocyte pyroptosis in knee osteoarthritis by targeting SMAD2 and inhibiting the NLRP3/Caspase-1 pathway

MicroRNA-155 regulates osteogenesis and bone mass phenotype via targeting S1PR1 gene

Reduced miR‑519d‑3p levels in the synovium and synovial fluid facilitate the progression of post‑traumatic osteoarthritis by targeting VEGF

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