• 제목/요약/키워드: chondrocyte

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Effect of low intensity pulsed ultrasound in activating the mitogen-activated protein kinase signaling pathway and inhibition inflammation cytokine synthesis in chondrocytes

  • Kim, Eun-Jung;Kim, Gye-Yeop
    • Physical Therapy Rehabilitation Science
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    • v.3 no.1
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    • pp.33-37
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    • 2014
  • Objective: Low intensity pulsed ultrasound (LIPUS) has been shown to accelerate cell proliferation and tissue healing in both animal models and clinical trials. However, details of the clinical effects of LIPUS have not been well characterized. The aim of this study was to investigate the effect of LIPUS on mitogen-activated protein kinase (MAPK) activation in rat articular chondrocytes. Design: Cross-sectional study. Methods: Chondrocyte were cultured in six well cell culture plates for 72 hours at $37^{\circ}C$ with 5% $CO_2$, and then exposed to LIPUS at 1.5 MHz frequency and $30-mW/cm^2$ power. Changes in chondrocyte activities were evaluated in response to oxydative stress in dose-dependent (0 and 300 uM) and time-dependent (0-24 hr) manner. The cell viability were analyzed using MTT [3-(4.5-dimethylthiazol-2-yl)-2.5 diphenyltetrazolium bromide]. The expression of p38 MAPK was measured using western blotting. Results: Oxidative stress was induced in rat chondrocytes using hydrogen peroxide ($H_2O_2$). The cell viability was decreased in chondrocytes after the $H_2O_2$ dose and time-dependent treatment. The p38 MAPK phosphorylation occurred at a significantly increased rate after $H_2O_2$ treated (p<0.05). Expression of p38 MAPK was decreased in the p38 inhibitor groups compared with the oxidative stress-induced chondrocyte damage via the p38 MAPK signaling pathways (p<0.05). Conclusions: It could be concluded that LIPUS can inhibit oxidative stress-induced chondrocyte damage via the p38 MAPK signaling pathways.

Effects of cis-Dichlorodiammineplatinum (II) on the Epiphyseal Plate of the Tibia in the Albino Rat (cis-Dichlorodiammineplatinum (II)이 흰쥐 경골의 골단연골판에 미치는 영향)

  • Kim, Jong-Kwan;Kim, Won-Kyu;Chung, Ho-Sam
    • Applied Microscopy
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    • v.26 no.2
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    • pp.197-206
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    • 1996
  • cis-Dichlorodiammineplatinum (II) (cis-Platin) inhibits the proliferation and growth of the tumor cells by way of inhibiting DNA and protein synthesis of the cancer cells. Although cis-Platin is very effective antitumor drug, it also produces many other side effects. Thus the author has studied the effects of cis-Platin on the proximal epiphyseal plate in the tibia of the rat. The results were as follows: In the chondrocyte of the proliferative zone, sacculated, and fragmented cisternae of rough endoplasmic reticulum, some mitochondria with disorganized mitochondrial cristae and distorted procollagens were observed, and in the matrix some large matrix granules and dispersed collagen fibrils were revealed on the 1st, 3rd day and 1st week group of cis-Platin treated rats. In the chondrocyte of the proliferative zone of cis-Platin treated rats on the 2nd and 3rd week group, parallely arranged rough endoplasmic reticulum and many procollagens were shown, and in the matrix a number of large matrix granules and many small matrical granules as well as collagen fibrils were revealed. Consequently it is suggested that though cis-Platin induces the degenerative changes of the chondrocyte resulting in components of the cartilagenous matrix, these toxic effects are regressed with time.

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A77 1726 Inhibit NO-induced Apoptosis via PI-3K/AKT Signaling Pathway in Rabbit Articular Chondrocyte

  • Choi, In-Kyou;Kim, Song-Ja
    • Biomedical Science Letters
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    • v.15 no.1
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    • pp.61-66
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    • 2009
  • Leflunomide is an immunomodulatory agent used for the treatment of rheumatoid arthritis (RA). Leflunomide known as a regulator of iNOS synthesis which largely decreases NO production in diverse cell type. However, the effect of leflunomide on chondrocyte is still poorly understood. In our previous studies, we have shown that direct production of Nitric oxide (NO) by treating chondrocytes with NO donor, sodium nitroprusside (SNP), causes apoptosis via p38 mitogen-activated protein kinase in association with elevation of p53 protein level, caspase-3 activation. In this study, we characterized the molecular mechanism by which A77 1726 inhibit apoptosis. We found that A77 1726 inhibit NO-induced apoptosis as determined by MTT (Thiazolyl Blue Tetrazolium Bromide) assay and DNA fragmentation. The inhibition of apoptosis by A77 1726 was accompanied by increased PI-3 kinase and AKT activities. So, inhibition of phosphatidylinositol (PI)-3kinase with LY294002 rescued apoptosis. Triciribine, the specific inhibitor of AKT, also abolished anti-apoptotic effect. Our results indicate that A77 1726, the active metabolite of leflunomide, mediates NO-induced apoptosis in chondrocytes by modulating up-regulation of PI-3 kinase and AKT.

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Extracts of Sorbus commixta and Geranium thunbergii inhibit Osteoclastogenesis and stimulate Chondrogenesis (마가목 및 현지초 추출물의 골손실 및 연골손상 억제효과)

  • Moon, Eun-Jung;Youn, You-Suk;Choi, Bo-Yun;Jeong, Hyun-Uk;Park, Ji-Ho;Oh, Myung-Sook;Soh, Yun-Jo;Kim, Sun-Yeou
    • Journal of the Korea Academia-Industrial cooperation Society
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    • v.11 no.9
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    • pp.3358-3365
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    • 2010
  • This study was carried out to investigate the effect of Sorbus commixta (SC), Geranium thunbergii (GT) and their mixture (SC:GT=1:1, MIX) on inhibition of bone loss and chondral defect. To examine their activities, we measured the alkaline phosphatase (ALP) activity in human osteoblast-like MG-63 cells and performed tartrate-resistant acid phosphate (TRAP) staining in osteoclast differentiated from Raw264.7 cells. To investigate the influence on chondrocyte differentiation, we performed alcian-blue staining in chondrocyte differentiated from ATDC5 cells. All of SC, GT and MIX did not increase ALP activity in MG-63 cells. However, SC and mixture (SC:GT=1:1, MIX) significantly inhibited osteoclastic differentiation. And they also induced chondrocyte differentiation. These results suggest that SC and GT may have a potential for the treatment of bone loss and chondral defect by suppression of osteoclast differentiation and stimulation of chondrocyte differentiation. Therefore, clarification of their mechanisms and active components will be needed.

Second Look Arthroscopic Finding after Fibrin Matrix Autologous Chondrocyte Implantation for the Treatment of Articular Cartilage Defect of the Knee - Preliminary Report - (슬관절 연골 결손에 대한 fibrin matrix 자가 연골 세포 이식술 후 이차 관절경 소견 - 예비보고 -)

  • Choi, Sung-Wook;Oh, In-Suk;Kim, Ryuh-Sup;Park, Sun-Won;Lee, Jong-Min;Lee, Moon;Kim, Myung-Ku
    • Journal of the Korean Arthroscopy Society
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    • v.11 no.1
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    • pp.1-6
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    • 2007
  • Purpose: The purpose of this preliminary report is to investigate the short term outcome of performing gel type fibrin matrix autologous chondrocyte implantation to patients who have damaged knee joint cartilage using secondary arthroscopy. Material and Methods: Six patients who have damaged knee joint cartilage were involved. The average size of defect was $5.13\;cm^2$. While performing primary arthroscopy, whole layer of cartilage bone was obtained either from the margin of damaged cartilage or the bilateral margin of a trochlea. The cartilaginous cells were obtained for culture for four to six weeks. While performing secondary minimal invasive arthrotomy, gel type fibrin matrix autologous chondrocyte was implanted on the chondral defect site. Results: 4 among 6 patients to be more than good in Modified Cincinnati Knee Scoring system. Lysholm function score was 59.5 preoperatively, and it improved to 76.25. ICRS grading by performing secondary arthroscopy revealed 4 out of 6 patients to be nearly normal. Conclusion: Gel type fibrin matrix autologous chondrocyte implantation is a treatment for cartilage defect, which takes less time to operate than the conventional implantation. In addition, this method minimizes the size of incision and allows arthroscopic surgery. However, long term follow up and more case study is thought to be necessary.

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Adhesion Strength Measurement of Rabbit Knee Chondrocyte (연골세포 부착력 평가)

  • Lee Kwon-Yong;Park Sang-Guk;Shin Daehwan;Park Jong-Chul
    • Tribology and Lubricants
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    • v.21 no.5
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    • pp.236-240
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    • 2005
  • In order to prepare for the suitable surfaces of implants or medical devices, quantitative evaluation of adhesion between cells and biomaterials is essential. To better understand adhesion formation between cells and biomaterials, we used the cytodetachment technique which measures the adhesive force of a single cell through changing the, culture time and detachment speed. The results showed that the adhesive force could be affected by the culture time of cells on the surface of materials and the detachment speed. Moreover, there was a large discrepancy among the adhesion strength measured by similar techniques conducted on the different cells and substrates. It can be 'concluded that the variation of the force measurement technique can seriously alter the level of the force required to detach a cell on the surface of materials.

Cartilage tissue engineering for craniofacial reconstruction

  • Kim, Min-Sook;Kim, Hyung-Kyu;Kim, Deok-Woo
    • Archives of Plastic Surgery
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    • v.47 no.5
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    • pp.392-403
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    • 2020
  • Severe cartilage defects and congenital anomalies affect millions of people and involve considerable medical expenses. Tissue engineering offers many advantages over conventional treatments, as therapy can be tailored to specific defects using abundant bioengineered resources. This article introduces the basic concepts of cartilage tissue engineering and reviews recent progress in the field, with a focus on craniofacial reconstruction and facial aesthetics. The basic concepts of tissue engineering consist of cells, scaffolds, and stimuli. Generally, the cartilage tissue engineering process includes the following steps: harvesting autologous chondrogenic cells, cell expansion, redifferentiation, in vitro incubation with a scaffold, and transfer to patients. Despite the promising prospects of cartilage tissue engineering, problems and challenges still exist due to certain limitations. The limited proliferation of chondrocytes and their tendency to dedifferentiate necessitate further developments in stem cell technology and chondrocyte molecular biology. Progress should be made in designing fully biocompatible scaffolds with a minimal immune response to regenerate tissue effectively

Paclitaxel Suppress Dedifferentiation via Mitogen-activated Protein Kinase Pathway in Rabbit Articular Chondrocyte

  • Im, Jeong-Hee;Kim, Song-Ja
    • Biomedical Science Letters
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    • v.15 no.1
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    • pp.67-72
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    • 2009
  • Microtubule-interfering agents (MIAs), including paclitaxel, have been attributed in part to interference with microtubule assembly, impairment of mitosis, and changes in cytoskeleton. But the signaling mechanisms that link microtubule disarray to destructive or protective cellular responses are poorly understood. This study investigated the effect of paclitaxel on differentiation such as type II collagen expression and sulfated proteoglycan accumulation in rabbit articular chondrocytes. Paclitaxel caused differentiated chondrocyte phenotype as demonstrated by increment of type II collagen expression and proteoglycan synthesis Paclitaxel treatment stimulated activation of ERK-1/2 and p38 kinase. Inhibition of ERK-1/2 with PD98059 enhanced paclitaxel-induced differentiation, whereas inhibition of p38 kinase with SB203580 suppressed paclitaxel-induced differentiation. Our findings suggest that ERK-1/2 and p38 kinase oppositely regulate paclitaxel-induced differentiation in chondrocytes.

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Latent Transforming Growth Factor-beta1 Functionalised Electrospun Scaffolds Promote Human Cartilage Differentiation: Towards an Engineered Cartilage Construct

  • Lim, Erh-Hsuin;Sardinha, Jose Paulo;Myers, Simon;Stevens, Molly
    • Archives of Plastic Surgery
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    • v.40 no.6
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    • pp.676-686
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    • 2013
  • Background To overcome the potential drawbacks of a short half-life and dose-related adverse effects of using active transforming growth factor-beta 1 for cartilage engineering, a cell-mediated latent growth factor activation strategy was developed incorporating latent transforming growth factor-${\beta}$1 (LTGF) into an electrospun poly(L-lactide) scaffold. Methods The electrospun scaffold was surface modified with NH3 plasma and biofunctionalised with LTGF to produce both random and orientated biofunctionalised electrospun scaffolds. Scaffold surface chemical analysis and growth factor bioavailability assays were performed. In vitro biocompatibility and human nasal chondrocyte gene expression with these biofunctionalised electrospun scaffold templates were assessed. In vivo chondrogenic activity and chondrocyte gene expression were evaluated in athymic rats. Results Chemical analysis demonstrated that LTGF anchored to the scaffolds was available for enzymatic, chemical and cell activation. The biofunctionalised scaffolds were non-toxic. Gene expression suggested chondrocyte re-differentiation after 14 days in culture. By 6 weeks, the implanted biofunctionalised scaffolds had induced highly passaged chondrocytes to re-express Col2A1 and produce type II collagen. Conclusions We have demonstrated a proof of concept for cell-mediated activation of anchored growth factors using a novel biofunctionalised scaffold in cartilage engineering. This presents a platform for development of protein delivery systems and for tissue engineering.