A5015590017- Osteoarthritis Treatment and Mechanisms
- Inflammatory mediators and NSAID effects
- Cell Adhesion Molecules Research
- Protein Kinase Regulation and GTPase Signaling
- Cytokine Signaling Pathways and Interactions
- NF-κB Signaling Pathways
- Chemokine receptors and signaling
- Protease and Inhibitor Mechanisms
- Peroxisome Proliferator-Activated Receptors
- Immune Response and Inflammation
- Ubiquitin and proteasome pathways
- Wnt/β-catenin signaling in development and cancer
- Trace Elements in Health
- interferon and immune responses
- Cellular Mechanics and Interactions
- Cancer-related molecular mechanisms research
- Cancer, Hypoxia, and Metabolism
- Fibroblast Growth Factor Research
- Proteoglycans and glycosaminoglycans research
- Tendon Structure and Treatment
- Connective tissue disorders research
- Adipose Tissue and Metabolism
- Sphingolipid Metabolism and Signaling
- RNA Research and Splicing
- Cancer-related gene regulation
Gwangju Institute of Science and Technology
2015-2024
Creative Research
2019
Intel (United States)
2008
Howard University
2003
Kyungpook National University
1995-2002
University of Massachusetts Amherst
1992-1993
Columbia University
1991
Howard Hughes Medical Institute
1991
Nitric oxide regulates cartilage destruction by causing dedifferentiation and apoptosis of chondrocytes. We investigated the role mitogen-activated protein kinase subtypes, extracellular signal-regulated (ERK)-1/2, p38 in NO-induced rabbit articular chondrocytes their involvement dedifferentiation. Generation NO with sodium nitroprusside (SNP) caused dedifferentiation, as indicated inhibition type II collagen expression proteoglycan synthesis. additionally apoptosis, accompanied p53...
Two key process features that are used to make 45 nm generation metal gate + high-k dielectric CMOS transistors highlighted in this paper. The first feature is the integration of stress-enhancement techniques with dual metal-gate transistors. second extension 193 dry lithography technology node pitches. Use these has enabled industry-leading transistor performance and high volume technology.
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...
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...
Nitric oxide (NO) during primary culture of articular chondrocytes causes apoptosis via p38 mitogen-activated protein kinase in association with elevation p53 level, caspase-3 activation, and differentiation status. In this study, we characterized the molecular mechanism by which induces through activation p53. We report here that NO-induced leads to NFkappaB, turn transcription gene. Activated also physically associates phosphorylates serine 15 residue p53, results accumulation apoptosis....
Cartilage development is initiated by the differentiation of mesenchymal cells into chondrocytes. Differentiated chondrocytes in articular cartilage undergo dedifferentiation and apoptosis during arthritis, which NO production plays a critical role. Here, we investigated roles mechanisms action insulin-like growth factor-1 (IGF-1) chondrogenesis maintenance survival differentiated IGF-1 induced limb bud micromass culture through activation phosphatidylinositol 3-kinase (PI3K) Akt. PI3K...
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...
In obesity, adipose tissue macrophages (ATMs) play a key role in mediating proinflammatory responses the tissue, which are associated with obesity-related metabolic complications. Recently, hypoxia has been implicated regulation of ATMs obesity. However, hypoxia-inducible factor (HIF)-2α, one major transcription factors induced by hypoxia, not fully elucidated ATMs. this study, we demonstrate that elevation macrophage HIF-2α would attenuate inflammation and improve insulin resistance...
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...
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...
Abstract Background This study was performed to develop therapeutic targets of osteoarthritis (OA) that can be targeted alleviate OA development (i.e., cartilage destruction) and relieve the OA-associated joint pain. Methods The candidate molecule, STING (stimulator interferon genes, encoded by Sting1), identified microarray analysis OA-like mouse chondrocytes. Experimental in mice induced destabilization medial meniscus (DMM). functions hindpaw mechanical allodynia were evaluated...
Interleukin (IL)-1β is a major catabolic cytokine that plays pivotal role in cartilage destruction. This study examined the possible involvement and regulatory mechanisms of Wnt signaling IL-1β-induced inhibition type II collagen expression chondrocytes. Treatment chondrocytes with IL-1β up-regulated Wnt-5a down-regulated Wnt-11 expression. Conditioned medium from Wnt-5a-expressing cells inhibited expression, whereas knockdown by siRNA blocked inhibitory effects on In contrast to Wnt-5a,...
Our previous study indicated that interleukin (IL)‐1β induces expression of several Wnt proteins in chondrocytes and causes chondrocyte dedifferentiation via the c‐Jun/activator protein‐1 (AP‐1) pathway. This examined whether Wnt‐3a c‐Jun/AP‐1 inhibited chondrogenesis mesenchymal cells by stabilizing cell–cell adhesion a manner independent β‐catenin transcriptional activity. also induced articular stimulating activity β‐catenin‐T cell‐factor/lymphoid‐enhancer‐factor (Tcf/Lef) complex. In...
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...
Objective Osteoarthritis (OA) is initiated by pathogenic factors produced multiple stimuli, including mechanical stress, metabolic and/or inflammaging. This study was undertaken to identify novel low‐grade inflammation–associated mediators of OA. Methods Candidate molecules were screened using microarray data obtained from chondrocytes exposed OA‐associated catabolic factors. In mice with OA generated destabilization the medial meniscus (DMM), inflammation induced a high‐fat diet or...