Primary chondrocytes enhance cartilage tissue formation upon co-culture with a range of cell types

Soft Matter ◽  
2010 ◽  
Vol 6 (20) ◽  
pp. 5080 ◽  
Author(s):  
Jeanine A. A. Hendriks ◽  
Razvan L. Miclea ◽  
Roka Schotel ◽  
Ewart de Bruijn ◽  
Lorenzo Moroni ◽  
...  
2015 ◽  
Vol 21 (3-4) ◽  
pp. 683-693 ◽  
Author(s):  
Drew W. Taylor ◽  
Nazish Ahmed ◽  
Justin Parreno ◽  
Gregory P. Lunstrum ◽  
Allan E. Gross ◽  
...  

2020 ◽  
Vol 17 (1) ◽  
pp. 54
Author(s):  
Nazem Ghasemi ◽  
Arefeh Basiri ◽  
Batool Hashemibeni ◽  
Mohammad Kazemi ◽  
Ali Valiani ◽  
...  

2018 ◽  
Vol 77 ◽  
pp. 48-62 ◽  
Author(s):  
Fanyi Li ◽  
Vinh X. Truong ◽  
Philipp Fisch ◽  
Clara Levinson ◽  
Veronica Glattauer ◽  
...  

2020 ◽  
Vol 21 (2) ◽  
pp. 581 ◽  
Author(s):  
Phoonsuk Limraksasin ◽  
Takeru Kondo ◽  
Maolin Zhang ◽  
Hiroko Okawa ◽  
Thanaphum Osathanon ◽  
...  

Cell condensation and mechanical stimuli play roles in osteogenesis and chondrogenesis; thus, they are promising for facilitating self-organizing bone/cartilage tissue formation in vitro from induced pluripotent stem cells (iPSCs). Here, single mouse iPSCs were first seeded in micro-space culture plates to form 3-dimensional spheres. At day 12, iPSC spheres were subjected to shaking culture and maintained in osteogenic induction medium for 31 days (Os induction). In another condition, the osteogenic induction medium was replaced by chondrogenic induction medium at day 22 and maintained for a further 21 days (Os-Chon induction). Os induction produced robust mineralization and some cartilage-like tissue, which promoted expression of osteogenic and chondrogenic marker genes. In contrast, Os-Chon induction resulted in partial mineralization and a large area of cartilage tissue, with greatly increased expression of chondrogenic marker genes along with osterix and collagen 1a1. Os-Chon induction enhanced mesodermal lineage commitment with brachyury expression followed by high expression of lateral plate and paraxial mesoderm marker genes. These results suggest that combined use of micro-space culture and mechanical stimuli facilitates hybrid bone/cartilage tissue formation from iPSCs, and that the bone/cartilage tissue ratio in iPSC constructs could be manipulated through the induction protocol.


2009 ◽  
Vol 15 (3) ◽  
pp. 665-673 ◽  
Author(s):  
Nazish Ahmed ◽  
Lu Gan ◽  
Andras Nagy ◽  
Jianing Zheng ◽  
Chen Wang ◽  
...  

Molecules ◽  
2021 ◽  
Vol 26 (19) ◽  
pp. 5732
Author(s):  
Jianjing Lin ◽  
Li Wang ◽  
Jianhao Lin ◽  
Qiang Liu

Articular cartilage (AC) damage is quite common, but due to AC’s poor self-healing ability, the damage can easily develop into osteoarthritis (OA). To solve this problem, we developed a microsphere/hydrogel system that provides two growth factors that promote cartilage repair: transforming growth factor-β3 (TGF-β3) to enhance cartilage tissue formation and ghrelin synergy TGF-β to significantly enhance the chondrogenic differentiation. The hydrogel and microspheres were characterized in vitro, and the biocompatibility of the system was verified. Double emulsion solvent extraction technology (w/o/w) is used to encapsulate TGF-β3 and ghrelin into microspheres, and these microspheres are encapsulated in a hydrogel to continuously release TGF-β3 and ghrelin. According to the chondrogenic differentiation ability of mesenchymal stem cells (MSCs) in vitro, the concentrations of the two growth factors were optimized to promote cartilage regeneration.


2019 ◽  
Author(s):  
Ilona Uzieliene ◽  
Eiva Bernotiene ◽  
Greta Urbonaite ◽  
Jaroslav Denkovskij ◽  
Edvardas Bagdonas ◽  
...  

Abstract Aging is associated with the development of various chronic diseases, in which both hypertension and osteoarthritis (OA) are dominant. Currently, there is no effective treatment for OA, whereas hypertension is often treated using L-type voltage-operated calcium channel (VOCC) blocking drugs, nifedipine being among the most classical ones. Although nifedipine together with other VOCC inhibitors plays an important role in people wellbeing, there are unresolved questions on its possible effect on cartilage tissue homeostasis and the development of OA. Due to that, the aim of this study was to analyse the effects of nifedipine on metabolic processes in human chondrocytes and bone marrow mesenchymal stem cells (BMMSCs). To analyze whether those events were mediated specifically through VOCC, agonist BayK8644 was used. Our results demonstrate that nifedipine downregulated chondrocyte proliferation rate as well as mitochondrial respiration and ATP production (Agilent Seahorse) in both cell types. Analysis of cartilage explant histological sections by electron microscopy also suggested that part of mitochondria lose their activity in response to nifedipine.However, switch of energetic metabolic pathway towards glycolytic was observed only in chondrocytes. Stimulation with either nifedipine or BayK8644 resulted in elevated production of collagen type II and proteoglycans in micromass cultures under chondrogenic condition, although the effects of VOCC inhibitor Bay8466 were less expressed. Nitric oxide (NO) activity, as measured by flow cytometry, was upregulated by nifedipine in BMMSCs and particularly chondrocytes, suggesting that NO at least in part may account for the effects of nifedipine on metabolism in both tested cell types.Taken together, we conclude that antihypertensive drug nifedipine inhibits mitochondrial respiration in both chondrocytes and BMMSCs and that these effects may be associated with increased NO accumulation and pro-inflammatory activity. Glycolytic capacity was enhanced only in chondrocytes, suggesting that these cells have the capacity to switch from oxidative phosphorylation to glycolysis and alter their metabolic activity in response to VOCC inhibition. Finally, nifedipine stimulated production of collagen type II and proteoglycans in both cell types, implying its potentially beneficial anabolic effects on articular cartilage. These results highlight a potential link between consumption of antihypertensive drugs and cartilage health


2020 ◽  
pp. 5-12
Author(s):  
Alina Samitova ◽  
Pavel Krylov

Currently, the interest in studying glucose as a signaling molecule and a regulator of chondrocyte metabolism is increasing significantly. There is little available data on chondrocytes’ ability to respond to extracellular glucose concentration changes that help them to avoid harmful effects resulting from the lack or accumulation of intracellular glucose. We have collected and analyzed the information about the mechanism of glucose influence on articular cartilage chondrocyte in this study. We have learned that chondrocytes adapt to both high and low glucose concentrations by modulating the synthesis and degradation of GluT1. Consequently, glucose in different concentrations affects many fundamental cellular functions such as the cartilage matrix synthesis and disruption, proliferation, differentiation, and apoptosis. To build a functional model of glucose participation in articular cartilage remodeling the exhaustive search and analysis of literature has been performed using open access resources. The scheme reflects key processes that have direct or indirect effects on the catabolic or anabolic function of chondrocytes. As a result, we have created a functional model that shows the effect of glucose on the suppression or expression of compounds that are actively involved in cartilage tissue remodeling. For example, these are compounds such as nitric oxide, aggrecans and type II collagen and others. Despite the role of glucose in energy metabolism in all cell types, including chondrocytes, high concentrations of glucose can also have a harmful effect. The advantage of this model is systematic data, which facilitates the perception of the results and their relevance.


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