scholarly journals BMP-5 expression increases during chondrocyte differentiation in vivo and in vitro and promotes proliferation and cartilage matrix synthesis in primary chondrocyte cultures

2007 ◽  
Vol 214 (1) ◽  
pp. 56-64 ◽  
Author(s):  
Geneviève Mailhot ◽  
Meiheng Yang ◽  
April Mason-Savas ◽  
Carole A. MacKay ◽  
Irwin Leav ◽  
...  
Keyword(s):  
Cartilage Matrix ◽  
Chondrocyte Differentiation ◽  
Matrix Synthesis ◽  
Chondrocyte Cultures ◽  
And Cartilage

Peptide-functionalized starPEG/heparin hydrogels direct mitogenicity, cell morphology and cartilage matrix distribution in vitro and in vivo

2017 ◽  
Vol 12 (1) ◽  
pp. 229-239 ◽  
Author(s):  
Eliane Hesse ◽  
Uwe Freudenberg ◽  
Thomas Niemietz ◽  
Carina Greth ◽  
Melanie Weisser ◽  
...  
Keyword(s):  
Cell Morphology ◽  
Cartilage Matrix ◽  
Matrix Distribution ◽  
And Cartilage

scholarly journals Silibinin protects against osteoarthritis through inhibiting the inflammatory response and cartilage matrix degradation in vitro and in vivo

Oncotarget ◽  
2017 ◽  
Vol 8 (59) ◽  
pp. 99649-99665 ◽  
Author(s):  
Wenhao Zheng ◽  
Zhenhua Feng ◽  
Yiting Lou ◽  
Chunhui Chen ◽  
Chuanxu Zhang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Cartilage Matrix ◽  
Matrix Degradation ◽  
And Cartilage

BMP2 Is Required for Postnatal Maintenance of Osteochondral Tissues of the Temporomandibular Joint

Cartilage ◽  
2020 ◽  
pp. 194760352098015
Author(s):  
Mara H. O’Brien ◽  
Eliane H. Dutra ◽  
Shivam Mehta ◽  
Po-Jung Chen ◽  
Sumit Yadav
Keyword(s):  
Age Groups ◽  
Mandibular Condyle ◽  
Bone Morphogenetic Protein 2 ◽  
Matrix Synthesis ◽  
Cartilage Growth ◽  
Chondrocyte Proliferation ◽  
Conditional Deletion ◽  
Morphogenetic Protein

Objective Bone morphogenetic protein 2 (BMP2) plays important roles in cartilage growth and development. Paradoxically, elevated levels of BMP2 leads to hypertrophic differentiation and osteoarthritis of cartilage. We examined the in vivo loss of BMP2 in cells expressing aggrecan of the mandibular condyle and knee. Design Three-week-old BMP2 flox/flox- CreER-positive mice and their Cre-negative littermates were treated with tamoxifen and raised until 3 or 6 months. We also investigated the direct effects of BMP2 on chondrocytes in vitro. Cells from the mandibular condyle of mice were treated with recombinant human BMP2 (rhBMP2) or rhNoggin (inhibitor of BMP2 signaling). Results Conditional deletion of BMP2 caused breakage of the cartilage integrity in the mandibular condyle of mice from both age groups, accompanied by a decrease in cartilage thickness, matrix synthesis, mineralization, chondrocyte proliferation, and increased expression of degeneration markers, while the effects at articular cartilage were not significant. In vitro results revealed that rhBMP2 increased chondrocyte proliferation, mineralization, and differentiation, while noggin induced opposite effects. Conclusions In conclusion, BMP2 is essential for postnatal maintenance of the osteochondral tissues of the mandibular condyle.

scholarly journals Tissue Engineering of Muscles and Cartilages Using Polyelectrolyte Hydrogels

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Hyuck Joon Kwon
Keyword(s):  
Tissue Engineering ◽  
In Vivo Studies ◽  
Current Status ◽  
Polyelectrolyte Gel ◽  
Polyelectrolyte Gels ◽  
Joint Surfaces ◽  
Functional Replacement ◽  
And Cartilage

The prevalent nature of osteoarthritis that causes the erosion of joint surfaces and loss of mobility and muscle dystrophy that weakens the musculoskeletal system and hampers locomotion underlies the importance of developing functional replacement or regeneration of muscle and cartilage tissues. Polyelectrolyte gels have high potential as cellular scaffolds due to characteristic properties similar to biological matrixes. A number of in vitro and in vivo studies demonstrated that polyelectrolyte gels are useful for replacement and regeneration of muscle and cartilage tissues. In addition, it was also found that polyelectrolyte gels have high biocompatibility, durability, and resistance to biodegradation. Moreover, polyelectrolyte gels can overcome their drawbacks of mechanical behavior by introducing double network into the gel. This paper reviews the current status and recent progress of polyelectrolyte gel-based tissue engineering for repairs of muscle and cartilage tissues.

scholarly journals Progress and Applications of Polyphosphate in Bone and Cartilage Regeneration

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Yan Wang ◽  
Min Li ◽  
Pei Li ◽  
Haijun Teng ◽  
Dehong Fan ◽  
...  
Keyword(s):  
Cartilage Regeneration ◽  
High Energy ◽  
Cartilage Defects ◽  
Artificial Bone ◽  
Cellular Mechanisms ◽  
Inorganic Polyphosphate ◽  
Morphogenetic Effects ◽  
And Cartilage

Patients with bone and cartilage defects due to infection, tumors, and trauma are quite common. Repairing bone and cartilage defects is thus a major problem for clinicians. Autologous and artificial bone transplantations are associated with many challenges, such as limited materials and immune rejection. Bone and cartilage regeneration has become a popular research topic. Inorganic polyphosphate (polyP) is a widely occurring biopolymer with high-energy phosphoanhydride bonds that exists in organisms from bacteria to mammals. Much data indicate that polyP acts as a regulator of gene expression in bone and cartilage tissues and exerts morphogenetic effects on cells involved in bone and cartilage formation. Exposure of these cells to polyP leads to the increase of cytokines that promote the differentiation of mesenchymal stem cells into osteoblasts, accelerates the osteoblast mineralization process, and inhibits the differentiation of osteoclast precursors to functionally active osteoclasts. PolyP-based materials have been widely reported in in vivo and in vitro studies. This paper reviews the current cellular mechanisms and material applications of polyP in bone and cartilage regeneration.

Dexamethasone induces apoptosis in proliferative canine tendon cells and chondrocytes

2008 ◽  
Vol 21 (04) ◽  
pp. 337-342 ◽  
Author(s):  
M. A. Hossain ◽  
J. Park ◽  
S. H. Choi ◽  
G. Kim
Keyword(s):  
Cell Proliferation ◽  
Cartilage Degeneration ◽  
Dependent Manner ◽  
Tendon Cells ◽  
Cartilage Cells ◽  
In Vitro Effects ◽  
Nuclear Apoptosis ◽  
And Cartilage

SummaryDexamethasone (Dexa) has been commonly used in humans and domestic animals, particularly in the treatment of tendon injuries and cartilage degeneration. However, it is often associated with tendon rupture and impaired tendon and cartilage healing. In the present study, we investigated Dexa’s in vitro effects on the growth of cell proliferation and the induction of apoptosis in canine Achilles tendon cells and chondrocytes. Cell proliferation after treatment with Dexa for two to six days was quantified by a 2,3-bis{2-methoxy- 4-nitro-5-sulfophenyl}-2H-tetrazolium-5-carboxyanilide inner salt assay (XTT). The results showed that Dexa could inhibit the proliferation of tendon cells and chondrocytes at increasing concentrations (0.1–50 μg/ml) compared with untreated cells. Cell apoptosis was induced by Dexa, as evidenced by the typical nuclear apoptosis using Hoechst 33258 staining. Dexa increased the apoptosis of canine tendon cells and chondrocytes in a time-dependent manner. In canine tendon cells and chondrocytes that were treated with 25 and 50 μg/ml concentration of Dexa, the number of condensed apoptotic nuclei was significantly increased. In addition, culturing with Dexa and the glucocorticoid receptor blocker, mifepristone, significantly arrested apoptosis of tendon cells and chondrocytes. Based on our in vitro data, we hypothesized that in vivo treatment with glucocorticoids may diminish the proliferation of tendon and cartilage cells by increasing apoptosis and suppressing the proliferation. Our findings suggest that Dexa could be used with caution in dogs with articular or tendon problems.

scholarly journals Inhibition of SYK and cSrc kinases can protect bone and cartilage in preclinical models of osteoarthritis and rheumatoid arthritis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
F. N. Novikov ◽  
M. V. Panova ◽  
I. Y. Titov ◽  
V. S. Stroylov ◽  
O. V. Stroganov ◽  
...  
Keyword(s):  
Bone Tissue ◽  
In Vitro Models ◽  
Multikinase Inhibitor ◽  
Monosodium Iodoacetate ◽  
Disease Modifying ◽  
Cartilage Erosion ◽  
Disease Modifying Treatment ◽  
And Cartilage

AbstractThe pathophysiology of osteoarthritis (OA) includes the destruction of subchondral bone tissue and inflammation of the synovium. Thus, an effective disease-modifying treatment should act on both of these pathogenetic components. It is known that cSrc kinase is involved in bone and cartilage remodeling, and SYK kinase is associated with the inflammatory component. Thus the aim of this study was to characterize the mechanism of action and efficacy of a small molecule multikinase inhibitor MT-SYK-03 targeting SYK and cSrc kinases among others in different in vitro and in vivo arthritis models. The selectivity of MT-SYK-03 kinase inhibition was assayed on a panel of 341 kinases. The compound was evaluated in a set of in vitro models of OA and in vivo OA and RA models: surgically-induced arthritis (SIA), monosodium iodoacetate-induced arthritis (MIA), collagen-induced arthritis (CIA), adjuvant-induced arthritis (AIA). MT-SYK-03 inhibited cSrc and SYK with IC50 of 14.2 and 23 nM respectively. Only five kinases were inhibited > 90% at 500 nM of MT-SYK-03. In in vitro OA models MT-SYK-03 reduced hypertrophic changes of chondrocytes, bone resorption, and inhibited SYK-mediated inflammatory signaling. MT-SYK-03 showed preferential distribution to joint and bone tissue (in rats) and revealed disease-modifying activity in vivo by halving the depth of cartilage erosion in rat SIA model, and increasing the pain threshold in rat MIA model. Chondroprotective and antiresorptive effects were shown in a monotherapy regime and in combination with methotrexate (MTX) in murine and rat CIA models; an immune-mediated inflammation in rat AIA model was decreased. The obtained preclinical data support inhibition of cSrc and SYK as a viable strategy for disease-modifying treatment of OA. A Phase 2 clinical study of MT-SYK-03 is to be started.

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