MicroRNA221-3p modulates Ets-1 expression in synovial fibroblasts from patients with osteoarthritis of temporomandibular joint

Xu, Jie; Liu, Y.; Deng, Mohong; Li, Jianping; Cai, Hengxing; Meng, Qinggong; Fang, Wei; Long, Xing; Jin, Ke

doi:10.1016/j.joca.2016.06.011

Cited by 31 publications

(25 citation statements)

References 46 publications

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“…In addition, treatment with rIL-1β suppresses miR-221 expression in TMJ OA synovial fibroblasts. ETS1 , a transcription factor involved in MMP-1 , MMP-2 and MMP-9 expression, has been identified as direct miR-221 target in TMJ OA synovial fibroblasts [224]. Interestingly, increasing BMI has also been linked to reduced miR-221 abundance [225].…”

Section: Mirna Regulation Of Fibroblast Growth Factor 2 Transformmentioning

confidence: 99%

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

Boehme,

Rolauffs

2018

IJMS

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Osteoarthritis (OA) is a degenerative whole joint disease, for which no preventative or therapeutic biological interventions are available. This is likely due to the fact that OA pathogenesis includes several signaling pathways, whose interactions remain unclear, especially at disease onset. Early OA is characterized by three key events: a rarely considered early phase of proliferation of cartilage-resident cells, in contrast to well-established increased synthesis, and degradation of extracellular matrix components and inflammation, associated with OA progression. We focused on the question, which of these key events are regulated by growth factors, inflammatory cytokines, and/or miRNA abundance. Collectively, we elucidated a specific sequence of the OA key events that are described best as a very early phase of proliferation of human articular cartilage (AC) cells and concomitant anabolic/catabolic effects that are accompanied by incipient pro-inflammatory effects. Many of the reviewed factors appeared able to induce one or two key events. Only one factor, fibroblast growth factor 2 (FGF2), is capable of concomitantly inducing all key events. Moreover, AC cell proliferation cannot be induced and, in fact, is suppressed by inflammatory signaling, suggesting that inflammatory signaling cannot be the sole inductor of all early OA key events, especially at disease onset.

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Section: Mirna Regulation Of Fibroblast Growth Factor 2 Transformmentioning

confidence: 99%

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

Boehme,

Rolauffs

2018

IJMS

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“…Many interesting investigations revealing microRNA influence upon metalloproteinase expression have been undertaken. For instance, miR‐106a regulates MMP‐2 expression modulating Ets‐1; similarly, miR‐221 regulates MMP‐1 expression via the same pathway . The aforementioned MMP‐9 is also downregulated by miR‐195, which has been discussed in the section about elastin .…”

Section: Extracellular Matrixmentioning

confidence: 93%

“…For instance, miR-106a regulates MMP-2 expression modulating Ets-1; similarly, miR-221 regulates MMP-1 expression via the same pathway. 72,73 The aforementioned MMP-9 is also downregulated by miR-195, which has been discussed in the section about elastin. 28 A network between metalloproteinases and microRNA molecules inhibiting their expression has been presented in Figure 3.…”

Section: ) and Extracellular Matrix Metalloproteinases Inducer (Emmpmentioning

confidence: 98%

MicroRNA regulation of extracellular matrix components in the process of atherosclerotic plaque destabilization

Kowara

Cudnoch‐Jędrzejewska

Opolski

et al. 2017

Clin Exp Pharma Physio

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SummaryThe process of atherosclerotic plaque destabilization, leading to myocardial infarction, is still not fully understood. The pathway -composed of structural and regulatory proteins of the extracellular matrix (ECM) such as collagen, elastin, small leucine-rich proteoglycans, metalloproteinases, cathepsins and serine proteases -is one potential way of atherosclerotic plaque destabilization. The expression of these proteins is controlled by different microRNA molecules. The goal of this paper is to summarize the current investigations and knowledge about ECM in the process of atherosclerotic plaque destabilization, giving special attention to epigenetic expression regulation by microRNA. K E Y W O R D Satherosclerosis, collagen, extracellular matrix, metalloproteinases, RNA interference

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“…These TMJ-SFs were cultured as described previously. 20 The study protocols were approved by the Ethics were stimulated with 10 000 ng/mL of leptin for 9/24 and 12/24 hours for mRNA examination and ELISA, respectively.…”

Section: Cell Culture and Stimulationmentioning

confidence: 99%

Elevated leptin levels in temporomandibular joint osteoarthritis promote proinflammatory cytokine IL‐6 expression in synovial fibroblasts

Xiong

et al. 2019

J Oral Pathology Medicine

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Background Leptin, through binding to its special receptor (Ob‐Rb), has potent effects on immunity and inflammation. This study measured the levels of leptin in the synovial fluid of patients with temporomandibular joint osteoarthritis (TMJ‐OA) and healthy controls, determined the expression of Ob‐Rb and explored the effects and signalling pathways involved in leptin‐induced proinflammatory cytokine interleukin (IL)‐6 production in TMJ synovial fibroblasts (TMJ‐SFs). Methods Synovial fluid samples were obtained from 16 patients with TMJ‐OA and seven healthy controls. Leptin levels were measured in synovial fluid using enzyme‐linked immunosorbent assay (ELISA). Ob‐Rb expression was determined by quantitative real‐time polymerase chain reaction (qRT‐PCR) and Western blot in cultured TMJ‐SFs. Small interfering RNA (siRNA) was transfected into the TMJ‐SFs to down‐regulate the expression of Ob‐Rb. qRT‐PCR and ELISA were used to determine the levels of proinflammatory cytokine IL‐6 in leptin‐stimulated TMJ‐SFs. The involved signalling pathways that mediate the leptin‐stimulated production of IL‐6 were investigated using specific signalling inhibitor analyses. Results Compared with healthy controls, patients with TMJ‐OA had significantly higher concentrations of leptin in their synovial fluid. The expression levels of Ob‐Rb mRNA and proteins were detected in the TMJ‐SFs. Leptin can stimulate the mRNA and protein expression of IL‐6 in TMJ‐SFs by binding with Ob‐Rb. The leptin‐induced production of IL‐6 by the TMJ‐SFs significantly decreased after exposure to siRNA targeting Ob‐Rb. Inhibiting JAK2/STAT3, p38 MAPK or PI3K/Akt substantially decreased leptin‐induced IL‐6 production. Conclusion Leptin may up‐regulate IL‐6 production in vitro by binding with Ob‐Rb in TMJ‐SFs via the activation of the JAK2/STAT3, p38 MAPK or PI3K/Akt signalling pathways.

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MicroRNA221-3p modulates Ets-1 expression in synovial fibroblasts from patients with osteoarthritis of temporomandibular joint

Abstract: The reduction of miRNA221-3p in synovial fibroblasts, attributed from abundance of IL-1β in inflamed circumstance, induces Ets-1 up-regulation and then, initiates MMP1 and MMP9 secretion, thereby leading to continuously pathological development in TMJOA.

Cited by 31 publications

References 46 publications

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

MicroRNA regulation of extracellular matrix components in the process of atherosclerotic plaque destabilization

Elevated leptin levels in temporomandibular joint osteoarthritis promote proinflammatory cytokine IL‐6 expression in synovial fibroblasts

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