Glucan HBP-A increase type II collagen expression of chondrocytes in vitro and tissue engineered cartilage in vivo

2013 ◽  
Vol 21 (3) ◽  
pp. 196-203 ◽  
Author(s):  
Yue-long Cao ◽  
Ting Liu ◽  
Jian Pang ◽  
Ning-yang Gao ◽  
Hong-sheng Zhan ◽  
...  
Keyword(s):  
Type Ii Collagen ◽  
Type Ii ◽  
Collagen Expression ◽  
Engineered Cartilage

scholarly journals Method for in vitro production of cartilage microtissues from scaffold-free spheroids composed of human adipose-derived stem cells

2020 ◽  
Vol 7 (4) ◽  
pp. 3697-3708
Author(s):  
Vy Thi-Kieu Tu ◽  
Ha Thi-Ngan Le ◽  
Xuan Hoang-Viet To ◽  
Phuc Dang-Ngoc Nguyen ◽  
Phat Duc Huynh ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cartilage Damage ◽  
Cartilage Regeneration ◽  
Type Ii Collagen ◽  
Adipose Derived Stem Cells ◽  
Type Ii ◽  
In Vitro Production ◽  
Engineered Cartilage

Introduction: Cartilage damage is one of the injuries that is difficult for the human body to self-repair due to the avascular and completely mature tissue with only few stem or progenitor cells present. Recently, some studies showed that engineered cartilage tissues could be used to treat or improve this injury. This study aimed to produce the cartilage microtissues from the differentiation of scaffold-free spheroids composed of human adipose-derived stem cells. Methods: Human adipose-derived stem cells (ADSCs) were isolated and expanded following the previously published study. They were then cultured in the non-adherent condition to produce spheroids. The spheroids of the ADSCs were collected and induced into cartilage microtissues in the inducible medium for 21 days. The cartilage microtissue was characterized by some cartilage phenotype markers, including the accumulation of extracellular matrix proteins (aggrecan, glycosaminoglycan, and type II collagen), and the expression of certain genes specific to chondrocytes (Sox9, Col2, Col1, and Acan). Results: The results showed that the expression of chondrocyte-specific genes gradually increased during the 21 days of culture for differentiation. On day 21, the microtissues expressed aggrecan, glycosaminoglycan, and type II collagen proteins. Conclusion: This study demonstrated that cartilage microtissues could easily be produced from scaffold-free spheroids from ADSCs. Thus, cartilage microtissues can be produced in this manner for in vivo transplantation to promote cartilage regeneration, or to produce cartilage tissues for in vitro studies.  

Type VI collagen expression is upregulated in the early events of chondrocyte differentiation

Development ◽  
1993 ◽  
Vol 117 (1) ◽  
pp. 245-251
Author(s):  
R. Quarto ◽  
B. Dozin ◽  
P. Bonaldo ◽  
R. Cancedda ◽  
A. Colombatti
Keyword(s):  
Suspension Culture ◽  
Type I Collagen ◽  
Type Ii Collagen ◽  
Type I ◽  
Type Ii ◽  
Type Vi Collagen ◽  
Full Spectrum ◽  
Collagen Expression ◽  
Hypertrophic Chondrocyte

Dedifferentiated chondrocytes cultured adherent to the substratum proliferate and synthesize large amounts of type I collagen but when transferred to suspension culture they decrease proliferation, resume the chondrogenic phenotype and the synthesis of type II collagen, and continue their maturation to hypertrophic chondrocyte (Castagnola et al., 1986, J. Cell Biol. 102, 2310–2317). In this report, we describe the developmentally regulated expression of type VI collagen in vitro in differentiating avian chondrocytes. Type VI collagen mRNA is barely detectable in dedifferentiated chondrocytes as long as the attachment to the substratum is maintained, but increases very rapidly upon passage of the cells into suspension culture reaching a peak after 48 hours and declining after 5–6 days of suspension culture. The first evidence of a rise in the mRNA steady-state levels is obtained already at 6 hours for the alpha 3(VI) chain. Immunoprecipitation of metabolically labeled cells with type VI collagen antibodies reveals that the early mRNA rise is paralleled by an increased secretion of type VI collagen in cell media. Induction of type VI collagen is not the consequence of trypsin treatment of dedifferentiated cells since exposure to the actin-disrupting drug cytochalasin or detachment of the cells by mechanical procedures has similar effects. In 13-day-old chicken embryo tibiae, where the full spectrum of the chondrogenic differentiation process is represented, expression of type VI collagen is restricted to the articular cartilage where chondrocytes developmental stage is comparable to stage I (high levels of type II collagen expression).(ABSTRACT TRUNCATED AT 250 WORDS)

Discovery and development of a type II collagen neoepitope (TIINE) biomarker for matrix metalloproteinase activity: From in vitro to in vivo

2007 ◽  
Vol 361 (1) ◽  
pp. 93-101 ◽  
Author(s):  
O.V. Nemirovskiy ◽  
D.R. Dufield ◽  
T. Sunyer ◽  
P. Aggarwal ◽  
D.J. Welsch ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Metalloproteinase Activity

Comparison of the Therapeutic Effects of Gold Nanoclusters and Gold Nanoparticles on Rheumatoid Arthritis

2019 ◽  
Vol 15 (11) ◽  
pp. 2281-2290 ◽  
Author(s):  
Yao Zhao ◽  
Zhesheng He ◽  
Ruoping Wang ◽  
Pengju Cai ◽  
Xiangchun Zhang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Au Nanoparticles ◽  
Type Ii Collagen ◽  
Therapeutic Effects ◽  
Type Ii ◽  
Au Clusters ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation and progressive cartilage and bone damage. In our previous studies, we found that Au clusters using glutathione as a template (GACs) produced profound anti-inflammatory effects in vitro on lipopolysaccharide (LPS)-induced inflammation in mouse macrophage RAW 264.7 cells and type II collagen-induced rat RA in vivo. In this study, we examined whether the template for Au clusters synthesis has an effect on its anti-inflammatory effect and whether Au nanoparticles with larger particle diameter produce the same anti-inflammatory effect. We synthesized Au clusters with bovine serum albumin (BSA) as a template (BACs), Au clusters with glutathione (GSH) as a template (GACs), and Au nanoparticles with glutathione as a template (GANs) and compared their anti-inflammatory effects in vitro and in vivo. These three Au nanomaterials can inhibit the production of lipopolysaccharide (LPS)-induced proinflammatory mediators and ameliorate type II collagen-induced rat RA. However, although the three Au nanomaterials produced similar anti-inflammatory effects, the GANs with larger particle sizes were less stable in vivo and accumulated in the peritoneum after intraperitoneal injection, resulting in poor absorption in vivo. The BACs showed relatively high liver accumulation due to the larger molecular weight of the outer shell. Therefore, we believe that the GACs are potential reliable nanodrugs for the treatment of RA.

scholarly journals TGFβ superfamily-dependent and osmolarity-mediated type II collagen expression by chondrocytes in vitro

2016 ◽  
Vol 7 ◽  
pp. 110
Author(s):  
Ufuk T. Timur ◽  
M. Caron ◽  
A. van der Windt ◽  
P. Emans ◽  
T. Welting ◽  
...  
Keyword(s):  
Type Ii Collagen ◽  
Type Ii ◽  
Collagen Expression ◽  
Tgfβ Superfamily

Inhibitory effects of polyphenol punicalagin on type-II collagen degradation in vitro and inflammation in vivo

2013 ◽  
Vol 205 (2) ◽  
pp. 90-99 ◽  
Author(s):  
Dinorah Jean-Gilles ◽  
Liya Li ◽  
V.G. Vaidyanathan ◽  
Roberta King ◽  
Bongsup Cho ◽  
...  
Keyword(s):  
Type Ii Collagen ◽  
Collagen Degradation ◽  
Type Ii ◽  
Inhibitory Effects

scholarly journals Preparation of EGCG decorated, injectable extracellular vesicles for cartilage repair in rat arthritis

2021 ◽  
Author(s):  
Changwei Song ◽  
Shibo Xu ◽  
Linna Chang ◽  
Xingjun Zhao ◽  
Xifan Mei ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Extracellular Vesicles ◽  
Animal Experiments ◽  
Measurement Data ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Egcg Treatment ◽  
Limited Mobility

Abstract Arthritis is a kind of chronic inflammatory autoimmune disease, which can destroy joint cartilage and bone, leading to joint pain, joint swelling, and limited mobility. Traditional therapies have many side effects or focus too much on anti-inflammation while neglecting joint repair. In this experiment, we combined EGCG (Epigallocatechin gallate) with extracellular vesicles derived from macrophages to treat rheumatoid arthritis. Sustained-release resulted in a significant decrease in chondrocyte expression of HIF-1α, a decrease in apoptosis-related proteins Cytochrome C, Caspase-3, Caspase-9, and Bax. Molecular biological analysis showed that extracellular vesicles-encapsulated EGCG (EVs-EGCG) more significantly upregulated type II collagen expression by about 1.8-fold than EGCG alone, which was more beneficial for arthritis repair. Animal experiments revealed that these EGCG-coated extracellular vesicles significantly reduced swelling, decreased synovial hyperplasia, repaired cartilage, and attenuated arthritis-related pathology scores in arthritic rats. Measurement data showed that EVs-EGCG treatment reduced joint swelling by approximately 39.5% in rheumatoid rats. In vitro studies have shown that this EVs-EGCG can increase the expression of cartilage type II collagen and reduce apoptosis of chondrocytes. Moreover, it was demonstrated in vivo experiments to reduce cartilage destruction in rheumatoid arthritis rats, providing a solution for the treatment of rheumatoid arthritis.

scholarly journals The Effect of Varying Concentrations and Application Periods of Chondroitinase ABC on Tissue-Engineered Cartilage

2014 ◽  
Vol 1 (1) ◽  
Author(s):  
Eric Tong ◽  
Grace D. O'Connell ◽  
Terri-Ann N. Kelly ◽  
Clark T. Hung
Keyword(s):  
Mechanical Properties ◽  
Articular Cartilage ◽  
Treatment Option ◽  
Type Ii Collagen ◽  
Treated Group ◽  
Cartilage Tissue ◽  
Type Ii ◽  
Chondroitinase Abc ◽  
Engineered Cartilage

Osteoarthritis, a chronic malady characterized by joint pain and swelling, is caused by damage to articular cartilage and is perpetuated by low-grade inflammation.  Treatments for osteoarthritis do exist, but many treatments focus on coping with the disease rather than curing it.  Surgical options that replace damaged cartilage tissue with that of donor cartilage tissue or cartilage tissue from other parts of articular joints face complications especially when the tissue is not of the correct size or does not have native-like properties. A more suitable treatment option for osteoarthritis is to develop an in vitro tissue-engineered cartilage construct that can be grown using the patient’s own cells and to surgically remove the patient’s damaged cartilage and replace it with the tissue-engineered cartilage. A challenge in developing such a treatment option is producing tissue-engineered cartilage with mechanical properties akin to those of native human articular cartilage. This challenge may be overcome by maximizing the production of type II collagen by the chondrocytes in vitro. One way to maximize collagen production is through the application of chondroitinase ABC, an enzyme which temporarily suppresses proteoglycans in the cartilage matrix to create more space for type II collagen to develop. In this study, two two levels of cABC treatment were applied (“high” and “low”) to cartilage tissue constructs. The “low” cABC treated group received daily feeding of 0.075 U/mL from day 14 to 21 followed by a replacement of chondrogenic media without cABC.  The “high” cABC treated group received a single addition of 0.15 U/mL from day 14 to 16 followed by a replacement of chondrogenic media without cABC.  At the end of 42 days, the constructs were subjected to mechanical testing and biochemical analyses. These analyses showed that the high cABC treatment yielded more native-like mechanical properties when compared to the low cABC treatment and the control results.  Biochemical and histological analyses confirmed that the proteoglycan and collagen II content were higher in the low and high cABC treated groups when compared to the control. All analyses show that the most efficient application of chondroitinase ABC is through a two day duration treatment of a higher concentration (0.15 U/mL).

A Novel in Vitro Model to Investigate Behavior of Articular Chondrocytes in Osteoarthritis

2009 ◽  
Vol 37 (2) ◽  
pp. 426-431 ◽  
Author(s):  
KENNETH S. RANKIN ◽  
RACHEL L. LAKEY ◽  
CRAIG H. GERRAND ◽  
ANDREW P. SPROWSON ◽  
ANDREW W. McCASKIE ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Articular Chondrocytes ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Transcriptional Expression ◽  
Matrix Metalloproteinase 1 ◽  
Standard Culture ◽  
Cells Cultured

Objective. To investigate in vivo simulation of the microenvironment in which osteoarthritis (OA) chondrocytes are cultured in vitro.Methods. Human articular chondrocytes were cultured under normoxic and hypoxic conditions. Cells were cultured on standard culture plastic or a porous polyHEMA surface that closely resembles the in vivo cartilage microarchitecture. Morphological changes to the cells were demonstrated by fluorescent staining with DAPI and vinculin. Proteoglycan and type II collagen protein levels were assessed using established techniques. Matrix metalloproteinase-1 (MMP-1) production was assessed by ELISA. The gene expression of type II collagen and SOX9 was measured using real-time polymerase chain reaction.Results. Cells grown on culture plastic were seen to be flat and hexagonal. Cells cultured on the porous polyHEMA surface exhibited morphology in keeping with the in vivo microenvironment. Glycosaminoglycan release in hypoxia was high from cells cultured on standard culture plastic. Transcriptional expression of type II collagen was upregulated in hypoxia and by culture on the polyHEMA surface. Transcriptional expression of SOX9 in hypoxia was upregulated compared to normoxia; no significant effect was seen by varying the culture surface. Translational expression of type II collagen was upregulated at 20% oxygen on the polyHEMA surface compared to culture plastic and this was related to MMP-1 expression.Conclusion. Culture of chondrocytes in hypoxia and on a porous surface simulates the in vivo microenvironment and illustrates the molecular mechanisms of OA.

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