Noggin Inhibits IL-1β and BMP-2 Expression, and Attenuates Cartilage Degeneration and Subchondral Bone Destruction in Experimental Osteoarthritis

Chien, Szu-Yu; Tsai, Chun‐Hao; Liu, Shan‐Chi; Huang, Chien-Chung; Lin, Tzu-Hung; Yang, Yuzhen; Tang, Chih‐Hsin

doi:10.3390/cells9040927

Cited by 66 publications

(55 citation statements)

References 90 publications

(177 reference statements)

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“…Indeed, irisin can stimulate browning of white adipocytes through p38 and ERK MAPK [35], promotes human umbilical vein endothelial cell proliferation through the ERK signaling pathway [36] and osteoblast proliferation and differentiation via activating the phosphorylation of p38 and ERK [19]. Moreover, these pathways have been directly implied in OA pathogenesis [37]. In osteoarthritic cartilage, excessive amounts of basic fibroblast growth factor are released upon mechanical loading and activate several transduction pathways involving different MAPK, including ERK and p38.…”

Section: Discussionmentioning

confidence: 99%

Irisin Recovers Osteoarthritic Chondrocytes In Vitro

Vadalà

Giacomo

Ambrosio

et al. 2020

Cells

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Physical exercise favors weight loss and ameliorates articular pain and function in patients suffering from osteoarthritis. Irisin, a myokine released upon muscle contraction, has demonstrated to yield anabolic effects on different cell types. This study aimed to investigate the effect of irisin on human osteoarthritic chondrocytes (hOAC) in vitro. Our hypothesis was that irisin would improve hOAC metabolism and proliferation. Cells were cultured in growing media and then exposed to either phosphate-buffered saline (control group) or human recombinant irisin (experimental group). Cell proliferation, glycosaminoglycan content, type II/X collagen gene expression and protein quantification as well as p38/extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase (MAPK), protein kinase B (Akt), c-Jun N-terminal kinase (JNK), and nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) involvement were evaluated. Furthermore, gene expression of interleukin (IL)-1 and -6, matrix metalloproteinase (MMP)-1 and -13, inducible nitric oxide synthase (iNOS), and tissue inhibitor of matrix metalloproteinases (TIMP)-1 and -3 were investigated following irisin exposure. Irisin increased hOAC cell content and both type II collagen gene expression and protein levels, while decreased type X collagen gene expression and protein levels. Moreover, irisin decreased IL-1, IL-6, MMP-1, MMP-13 and iNOS gene expression, while increased TIMP-1 and TIMP-3 levels. These effects seemed to be mediated by inhibition of p38, Akt, JNK and NFκB signaling pathways. The present study suggested that irisin may stimulate hOAC proliferation and anabolism inhibiting catabolism through p38, Akt, JNK, and NFκB inactivation in vitro, demonstrating the existence of a cross-talk between muscle and cartilage.

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Section: Discussionmentioning

confidence: 99%

Irisin Recovers Osteoarthritic Chondrocytes In Vitro

Vadalà

Giacomo

Ambrosio

et al. 2020

Cells

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“…The details of the OA model and micro-computed tomography (micro-CT) assessment have been described in our previous publication [ 23 , 24 ]. Male Sprague-Dawley (SD) rats (8 weeks of age, weighing 300–350 g) were chosen for our OA model.…”

Section: Methodsmentioning

confidence: 99%

Resistin Enhances VCAM-1 Expression and Monocyte Adhesion in Human Osteoarthritis Synovial Fibroblasts by Inhibiting MiR-381 Expression through the PKC, p38, and JNK Signaling Pathways

Chen

Lin

Kuo

et al. 2020

Cells

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The development of osteoarthritis (OA) is characterized by synovial inflammation and the upregulation of vascular cell adhesion molecule type 1 (VCAM-1) in human osteoarthritis synovial fibroblasts (OASFs). This increase in VCAM-1 expression promotes monocyte adhesion to OASFs. The adipokine resistin is known to promote the release of inflammatory cytokines during OA progression. In this study, we identified significantly higher levels of resistin and CD68 (a monocyte surface marker) expression in human OA tissue compared with in healthy control tissue. We also found that resistin enhances VCAM-1 expression in human OASFs and facilitates the adhesion of monocytes to OASFs. These effects were attenuated by inhibitors of PKCα, p38, and JNK; their respective siRNAs; and by a microRNA-381 (miR-381) mimic. In our anterior cruciate ligament transection (ACLT) rat model of OA, the inhibition of resistin activity prevented ACLT-induced damage to the OA rat cartilage and pathological changes in resistin and monocyte expression. We also found that resistin affects VCAM-1 expression and monocyte adhesion in human OASFs by inhibiting miR-381 synthesis via the PKCα, p38, and JNK signaling pathways. Our clarification of the crucial role played by resistin in the pathogenesis of OA may lead to more effective therapy that reduces OA inflammation.

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“…Cd55 is a complement decay-accelerating factor in cartilage that play pivotal role in protecting chondrocytes from possible damage [50]. Nog serves as an inhibitor of bone morphogenetic proteins (BMPs), and prevents cartilage degeneration and osteoarthritis development by inhibiting Il1β and Bmp2 expression [51]. Esf1 is an essential nucleolar protein that is required for cartilage formation [52].…”

Section: Discussionmentioning

confidence: 99%

Insights Into the Molecular Mechanism of Deer Antler Extract Serving as a Potential Chondroprotective Agent for Articular Cartilage

Yao¹,

Zhou²,

Zhang³

et al. 2020

Preprint

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Background Deer antler is considered as a precious traditional Chinese medicinal material, and has been widely used to reinforce kidney’s yang, nourish essence and strengthen bone function. The most prominent bioactive components in deer antler are water-soluble proteins that play potential roles in bone formation and repair. The aim of this study was to explore the molecular control and therapeutic targets of deer antler extract (DAE) on articular cartilage. Methods DAE was prepared as previously described. All rats were randomly divided into Blank group and DAE group (10 rats per group) after 7-day adaptive feeding. The rats in DAE group were orally administrated with DAE at a dose of 0.2 g/kg per day for 3 weeks and the rats in Blank group were fed with drinking water. Total RNA was isolated from the articular cartilage of knee joints. RNA sequencing (RNA-seq) experiment combined with quantitative real-time polymerase chain reaction (qRT-PCR) verification assay were carried out to explore the molecular control and therapeutic targets of DAE on articular cartilage. Results We demonstrated that DAE played a potential role in promoting cartilage formation, growth and repair, and inhibiting cartilage degeneration and inflammation. These effects were possibly achieved by accelerating the expression of functional genes involved in chondrocyte commitment, survival, proliferation and differentiation, and suppressing the expression of susceptibility genes involved in the pathophysiology of osteoarthritis. Conclusions DAE might serve as a chondroprotective agent for treating cartilage degeneration and inflammation by boosting the ability of cartilage growth and repair. Thus, our findings will contribute towards deepening the knowledge about the molecular control and therapeutic targets of DAE on the treatment of osteoarthritis.

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Noggin Inhibits IL-1β and BMP-2 Expression, and Attenuates Cartilage Degeneration and Subchondral Bone Destruction in Experimental Osteoarthritis

Cited by 66 publications

References 90 publications

Irisin Recovers Osteoarthritic Chondrocytes In Vitro

Irisin Recovers Osteoarthritic Chondrocytes In Vitro

Resistin Enhances VCAM-1 Expression and Monocyte Adhesion in Human Osteoarthritis Synovial Fibroblasts by Inhibiting MiR-381 Expression through the PKC, p38, and JNK Signaling Pathways

Insights Into the Molecular Mechanism of Deer Antler Extract Serving as a Potential Chondroprotective Agent for Articular Cartilage

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