A5058821822- Osteoarthritis Treatment and Mechanisms
- Knee injuries and reconstruction techniques
- Total Knee Arthroplasty Outcomes
- Orthopaedic implants and arthroplasty
- Shoulder Injury and Treatment
- Cancer-related molecular mechanisms research
- Orthopedic Surgery and Rehabilitation
- Bone fractures and treatments
- Inflammatory mediators and NSAID effects
- Orthopedic Infections and Treatments
- Tendon Structure and Treatment
- Elbow and Forearm Trauma Treatment
- Peroxisome Proliferator-Activated Receptors
- Shoulder and Clavicle Injuries
- MicroRNA in disease regulation
- Circular RNAs in diseases
- Adhesion, Friction, and Surface Interactions
- RNA Research and Splicing
- NF-κB Signaling Pathways
- Sports injuries and prevention
- Hip and Femur Fractures
- Cell Adhesion Molecules Research
- Bone Metabolism and Diseases
- Nerve injury and regeneration
- Bone and Joint Diseases
Wonkwang University
2013-2022
Wonkwang University Medical Center
2011-2016
Yonsei University
2012
Growth Arrest-Specific 5 (GAS5) is known to negatively regulate cell survival and aberrantly expressed in several cancers. The influence of GAS5 on osteoarthritis (OA) has not been determined. To address this, articular chondrocytes were isolated from relatively normal (Non-OA) clear OA regions cartilage total knee replacement (TKR) patients biopsied cartilage. We found that was up-regulated compared with Non-OA chondrocytes. over-expression increased the expression levels MMPs, such as...
Hypoxia-inducible factor 2α (HIF-2α) (encoded by Epas1) causes osteoarthritic (OA) cartilage destruction regulating the expression of catabolic genes. We undertook this study to explore role interleukin-6 (IL-6) in HIF-2α-mediated OA mice.The HIF-2α, IL-6, and factors was determined at messenger RNA protein levels primary culture mouse chondrocytes, human cartilage, experimental cartilage. Experimental wild-type, HIF-2α-knockdown (Epas1+/-), Il6-/- mice caused intraarticular injection Epas1...
Apoptosis of articular chondrocytes is associated with the pathogenesis osteoarthritis (OA). Recently, we demonstrated that hypoxia-inducible factor (HIF)-2α, encoded by Epas1, causes OA cartilage destruction regulating expression various matrix-degrading enzymes. Here, investigated involvement HIF-2α in chondrocyte apoptosis and destruction. levels human mouse were markedly elevated association increased chondrocytes. Overexpression or knockdown alone did not cause apoptosis. However,...
Dkk is a family of canonical Wnt antagonists with 4 members (Dkk-1, Dkk-2, Dkk-3, and Dkk-4). We undertook this study to explore the roles Dkk-1 Dkk-2 in osteoarthritic (OA) cartilage destruction mice.Expression other catabolic factors was determined at messenger RNA protein levels human mouse OA cartilage. Experimental mice induced by destabilization medial meniscus (DMM) or intraarticular injection Epas1 adenovirus (AdEPAS-1). The role pathogenesis examined AdDkk-1 using...
<h3>Objective</h3> Hypoxia-inducible factor 2α (HIF-2α), encoded by <i>Epas1</i>, causes osteoarthritic cartilage destruction regulating the expression of matrix-degrading enzymes. We undertook this study to explore role nicotinamide phosphoribosyltransferase (NAMPT or visfatin) in HIF-2α-mediated destruction. <h3>Methods</h3> The HIF-2α, NAMPT and enzymes was determined at mRNA protein levels human osteoarthritis (OA) cartilage, mouse experimental OA primary cultured chondrocytes....
Osteoarthritis (OA) is characterized by impairment of the load-bearing function articular cartilage. OA cartilage matrix undergoes extensive biophysical remodeling decreased compliance. In this study, we elucidate mechanistic origin and downstream mechanotransduction pathway further demonstrate an active role mechanism in pathogenesis. Aging mechanical stress, two major risk factors OA, promote stiffening through accumulation advanced glycation end-products up-regulation collagen...
Abstract Here, in Ppara −/− mice, we found that an increased DNL stimulated the cartilage degradation and identified ACOT12 as a key regulatory factor. Suppressed level of was observed cartilages OA patient OA-induced animal. To determine role association pathogenesis, generated Acot12 knockout (KO) ( ) mice using RNA-guided endonuclease. displayed severe with stimulation matrix MMPs chondrocyte apoptosis through accumulation acetyl CoA. Delivery CoA-conjugated chitosan complex into...
beta-Catenin regulates important biological processes, including embryonic development and tumorigenesis. We have investigated the role of beta-catenin in regulation chondrocyte phenotype. Expression was high prechondrogenic mesenchymal cells, but significantly decreased differentiated chondrocytes both vivo vitro. Accumulation by inhibition glycogen synthase kinase-3beta with LiCl inhibited chondrogenesis stabilizing cell-cell adhesion. Conversely, low level articular increased...
Abstract Osteoclasts are multinucleated cells that formed by the fusion of mononuclear osteoclasts, which is an essential process in bone resorption leading to remodeling. Herein we show GM-CSF promoted prefusion osteoclasts (pOCs). The expression receptor-α was significantly up-regulated at stage pOCs induced RANKL. dendritic cell-specific transmembrane protein (DC-STAMP), mediated inducing NFATc1 via induction c-Fos. c-Fos and regulated ERK signaling pathway. Inhibition suppressed DC-STAMP...
Abstract Background Even though osteoarthritis (OA) is the most common musculoskeletal dysfunction, there are no effective pharmacological treatments to treat OA due lack of understanding in pathology. To better understand mechanism pathogenesis and investigate its target, we analyzed miRNA profiles during verify role functional targets miR-488. Results Human articular chondrocytes were obtained from cartilage patients undergoing knee replacement surgery biopsy samples normal expression...
Even though increasing evidences on miRNA involvement in human pathological responses, the distinct roles and related mechanisms of miRNAs pathology osteoarthritis (OA) are not yet fully understood.RNA levels or protein Apoptotic genes, HDACs, MMP-13, chondrocytes isolated from normal biopsy sample OA cartilages were analyzed by real-time PCR western blotting. Exogenous modulation miR-222 level was performed using delivery its specific precursor inhibitor target validation assay applied to...
Long non-coding RNAs (lncRNAs) have been reported to play important roles in cellular metabolism and development. Various diseases associated with aberrant expression of lncRNAs the related dysregulation mRNAs. An lncRNA profiling assay was carried out identify key osteoarthritic human synoviocytes; results revealed that prostate cancer gene marker 1 (PCGEM1) significantly overexpressed synoviocytes. Exogenous overexpression PCGEM1 inhibited apoptosis, induced autophagy, stimulated...
Hypoxia-inducible factor-2α (HIF-2α) is sufficient to cause experimental rheumatoid arthritis and acts regulate the functions of fibroblast-like cells from tissue surrounding joints, independent HIF-1α.
Osteoarthritis (OA) is a whole-joint disease characterized by cartilage destruction and other pathological changes. There currently no effective disease-modifying therapy. Here we investigate the post-transcriptional mRNA regulation of OA-modulating proteins in chondrocytes show that ZFP36 family member, ZFP36L1, specifically upregulated OA humans mice. Adenovirus-mediated overexpression ZFP36L1 alone mouse knee-joint tissue does not modulate pathogenesis. However, genetic ablation or...
The estrogen-related receptor (ERR) family of orphan nuclear is composed ERRα, ERRβ, and ERRγ, which are known to regulate various isoform-specific functions under normal pathophysiological conditions. Here, we investigate the involvement ERRs in pathogenesis osteoarthritis (OA) mice. Among ERR members, ERRγ markedly upregulated cartilage from human OA patients mouse models OA. Adenovirus-mediated overexpression knee joint or transgenic expression leads chondrocytes directly upregulates...
Osteoarthritis (OA) is the most common degenerative joint disease; however, its etiopathogenesis not completely understood. Here we show a role for NUDT7 in OA pathogenesis. Knockdown of normal human chondrocytes results disruption lipid homeostasis. Moreover, Nudt7-/- mice display significant accumulation lipids via peroxisomal dysfunction, upregulation IL-1β expression, and stimulation apoptotic death chondrocytes. Our genome-wide analysis reveals that knockout affects glycolytic pathway,...
The zinc-ZIP8-MTF1 axis induces metallothionein (MT) expression and is a catabolic regulator of experimental osteoarthritis (OA) in mice. main aim the current study was to explore roles underlying molecular mechanisms MTs OA pathogenesis.Experimental mice induced by destabilisation medial meniscus or intra-articular injection adenovirus carrying target gene (Ad-Zip8, Ad-Mtf1, Ad-Epas1, Ad-Nampt, Ad-Mt1 Ad-Mt2) into wild type, Zip8fl/fl; Col2a1-Cre, Mtf1fl/fl; Col2a1-Cre Mt1/Mt2 double...
Objective The basic leucine zipper transcription factor, ATF-like (BATF), a member of the Activator protein-1 family, promotes transcriptional activation or repression, depending on interacting partners (JUN-B C-JUN). Here, we investigated whether BATF/JUN complex exerts regulatory effects catabolic and anabolic gene expression in chondrocytes contributes to pathogenesis osteoarthritis (OA). Methods Primary cultured mouse were treated with proinflammatory cytokines (interleukin-1β, IL-6...
Summary The aim of this study was to determine the mechanism underlying association between one‐carbon metabolism and DNA methylation during chronic degenerative joint disorder, osteoarthritis ( OA ). Articular chondrocytes were isolated from human cartilage normal biopsied, degree degradation determined by safranin O staining. We found that expression levels SHMT ‐2 MECP increased in chondrocytes, 3′ UTR reporter assays showed are direct targets mi R ‐370 ‐373, respectively, articular...
Objective Osteoarthritis (OA) appears to be associated with various metabolic disorders, but the potential contribution of amino acid metabolism OA pathogenesis has not been clearly elucidated. Here, we explored whether alterations in chondrocytes could regulate pathogenesis. Methods Expression profiles metabolism-regulating genes primary-culture passage 0 mouse were examined by microarray analysis, and selected further characterised cartilage human models. Experimental mice was induced...