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

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.

The negatively charged microenvironment of collagen hydrogels regulates the chondrogenic differentiation of bone marrow mesenchymal stem cells in vitro and in vivo

2020 ◽  
Vol 8 (21) ◽  
pp. 4680-4693
Author(s):  
Jirong Yang ◽  
Yumei Xiao ◽  
Zizhao Tang ◽  
Zhaocong Luo ◽  
Dongxiao Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Protein Adsorption ◽  
Cell Morphology ◽  
Chondrogenic Differentiation ◽  
Collagen Hydrogels ◽  
Marrow Mesenchymal Stem Cells

The different negatively charged microenvironments of collagen hydrogels affect the protein adsorption, cell morphology, and chondrogenic differentiation of BMSCs in vitro and in vivo.

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 Functional Characterization of the Fission Yeast Phosphatidylserine Synthase Gene, pps1, Reveals Novel Cellular Functions for Phosphatidylserine

2007 ◽  
Vol 6 (11) ◽  
pp. 2092-2101 ◽  
Author(s):  
Yasuhiro Matsuo ◽  
Edward Fisher ◽  
Jana Patton-Vogt ◽  
Stevan Marcus
Keyword(s):  
Stationary Phase ◽  
Fission Yeast ◽  
Cell Morphology ◽  
Fluorescent Protein ◽  
Single Gene ◽  
Functional Characterization ◽  
Cellular Functions ◽  
Phosphatidylserine Synthase

ABSTRACT To investigate the contributions of phosphatidylserine to the growth and morphogenesis of the rod-shaped fission yeast Schizosaccharomyces pombe, we have characterized the single gene in this organism, pps1, encoding a predicted phosphatidylserine synthase. S. pombe pps1Δ mutants grow slowly in rich medium and are inviable in synthetic minimal medium. They do not produce detectable phosphatidylserine in vivo and possess negligible in vitro phosphatidylserine synthase activity, indicating that pps1 encodes the major phosphatidylserine synthase activity in S. pombe. Supplementation of growth medium with ethanolamine partially suppresses the growth-defective phenotype of pps1Δ cells, reflecting the likely importance of phosphatidylserine as a precursor for phosphatidylethanolamine in S. pombe. In medium lacking ethanolamine, pps1Δ mutants exhibit striking cell morphology, cytokinesis, actin cytoskeleton, and cell wall remodeling and integrity defects. Overexpression of pps1 likewise leads to defects in cell morphology and cytokinesis, thus implicating phosphatidylserine as a dosage-dependent regulator of these processes. During log-phase growth, green fluorescent protein-Pps1p fusion proteins are concentrated at the cell and nuclear peripheries as well as presumptive endoplasmic reticulum membranes, while in stationary-phase cells, they are redistributed to unusual cytoplasmic structures of unknown origin. Moreover, stationary-phase pps1Δ cultures retain very poor viability relative to wild-type S. pombe cells, even in medium containing ethanolamine, demonstrating a role for phosphatidylserine in the physiological adaptations required for stationary-phase survival. Our findings reveal novel cellular functions for phosphatidylserine and emphasize the usefulness of S. pombe as a model organism for elucidating potentially conserved biological and molecular functions of this phospholipid.

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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