Cross-linking affects cellular condensation and chondrogenesis in type II collagen-GAG scaffolds seeded with bone marrow-derived mesenchymal stem cells

2010 ◽  
Vol 28 (9) ◽  
pp. 1184-1192 ◽  
Author(s):  
Scott M. Vickers ◽  
Tobias Gotterbarm ◽  
Myron Spector
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Type Ii Collagen ◽  
Cross Linking ◽  
Type Ii ◽  
Cellular Condensation

scholarly journals Levels of matrix metalloproteinase-2 in committed differentiation of bone marrow mesenchymal stem cells induced by kartogenin

2019 ◽  
Vol 47 (7) ◽  
pp. 3261-3270
Author(s):  
Cheng Wang ◽  
Qiaohui Liu ◽  
Xiaoyuan Ma ◽  
Guofeng Dai
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Matrix Metalloproteinase ◽  
Type Ii Collagen ◽  
Matrix Metalloproteinase 2 ◽  
Type Ii ◽  
Proliferation And Differentiation ◽  
Marrow Mesenchymal Stem Cells

Objective To measure the inductive effect of kartogenin on matrix metalloproteinase-2 levels during the differentiation of human bone marrow mesenchymal stem cells (hMSCs) into chondrocytes in vitro. Methods In vitro cultured bone marrow hMSCs were grown to the logarithmic phase and then divided into three groups: control group (0 µM kartogenin), 1 µM kartogenin group and 10 µM kartogenin group. After 72 h of culture, cell proliferation and differentiation were observed microscopically. Matrix metalloproteinase-2 (MMP-2) in the cell supernatant and type II collagen levels in the cells were detected by enzyme linked immunosorbent assay and immunofluorescence staining, respectively. Results Kartogenin induced the proliferation and differentiation of hMSCs. With the increase of kartogenin concentration, the level of type II collagen was increased, while the level of MMP-2 decreased. Conclusion These findings indicate that kartogenin can induce hMSCs to differentiate into chondrocytes, and with the increase of kartogenin concentration, degeneration of the cartilage extracellular matrix may be inhibited.

scholarly journals Aqueous extract of Arctium lappa L. root (burdock) enhances chondrogenesis in human bone marrow-derived mesenchymal stem cells

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
King-Chuen Wu ◽  
Hung-Kai Weng ◽  
Yun-Shang Hsu ◽  
Pin-Jia Huang ◽  
Yang-Kao Wang
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Aqueous Extract ◽  
Chondrogenic Differentiation ◽  
Type Ii Collagen ◽  
Induction Medium ◽  
Type Ii ◽  
Arctium Lappa

Abstract Background Arctium lappa L. root (burdock root) has long been recommended for the treatment of different diseases in traditional Chinese medicine. Burdock root possesses anti-oxidative, anti-inflammatory, anti-cancer, and anti-microbial activities. The aim of the study was to elucidate whether aqueous extract of burdock root regulates mesenchymal stem cell proliferation and differentiation. Methods Human bone marrow-derived mesenchymal stem cells in 2D high density culture and in 3D micromass pellets were treated with chondrogenic induction medium and chondral basal medium in the absence or presence of aqueous extract of burdock root. The chondrogenic differentiation was accessed by staining glucosaminoglycans, immunostaining SOX9 and type II collagen and immuonblotting of SOX9, aggrecan and type II collagen. Results Treatment of aqueous extract of burdock root increased the cell proliferation of hMSCs. It did not have significant effect on osteogenic and adipogenic differentiation, but significantly enhanced chondrogenic induction medium-induced chondrogenesis. The increment was dose dependent, as examined by staining glucosaminoglycans, SOX9, and type II collagen and immunobloting of SOX9, aggrecan and type II collagen in 2D and 3D cultures. In the presence of supplemental materials, burdock root aqueous extract showed equivalent chondrogenic induction capability to that of TGF-β. Conclusions The results demonstrate that aqueous extract of Arctium lappa L. root promotes chondrogenic medium-induced chondrogenic differentiation. The aqueous extract of burdock root can even be used alone to stimulate chondrogenic differentiation. The study suggests that the aqueous extract of burdock root can be used as an alternative strategy for treatment purposes.

scholarly journals Type II Collagen-Conjugated Mesenchymal Stem Cells Micromass for Articular Tissue Targeting

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 880
Author(s):  
Shamsul Bin Sulaiman ◽  
Shiplu Roy Chowdhury ◽  
Mohd Fauzi Bin Mh Busra ◽  
Rizal Bin Abdul Rani ◽  
Nor Hamdan Bin Mohamad Yahaya ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Targeted Delivery ◽  
Expression Profiles ◽  
3D Culture ◽  
Type Ii Collagen ◽  
Cartilage Defects ◽  
Target Tissue ◽  
Type Ii ◽  
Antibody Conjugation

The tissue engineering approach in osteoarthritic cell therapy often requires the delivery of a substantially high cell number due to the low engraftment efficiency as a result of low affinity binding of implanted cells to the targeted tissue. A modification towards the cell membrane that provides specific epitope for antibody binding to a target tissue may be a plausible solution to increase engraftment. In this study, we intercalated palmitated protein G (PPG) with mesenchymal stem cells (MSCs) and antibody, and evaluated their effects on the properties of MSCs either in monolayer state or in a 3D culture state (gelatin microsphere, GM). Bone marrow MSCs were intercalated with PPG (PPG-MSCs), followed by coating with type II collagen antibody (PPG-MSC-Ab). The effect of PPG and antibody conjugation on the MSC proliferation and multilineage differentiation capabilities both in monolayer and GM cultures was evaluated. PPG did not affect MSC proliferation and differentiation either in monolayer or 3D culture. The PPG-MSCs were successfully conjugated with the type II collagen antibody. Both PPG-MSCs with and without antibody conjugation did not alter MSC proliferation, stemness, and the collagen, aggrecan, and sGAG expression profiles. Assessment of the osteochondral defect explant revealed that the PPG-MSC-Ab micromass was able to attach within 48 h onto the osteochondral surface. Antibody-conjugated MSCs in GM culture is a potential method for targeted delivery of MSCs in future therapy of cartilage defects and osteoarthritis.

Bone Marrow Mesenchymal Stem Cells (BMSCs) Transplantation Ameliorates Joint Severity and Inflammation in Rats with Arthritis

2022 ◽  
Vol 12 (5) ◽  
pp. 1028-1033
Author(s):  
Liangbang Wu ◽  
Zhenhai Hou ◽  
Longbao Zheng ◽  
Zenghui Gu
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Rat Model ◽  
Inflammatory Cells ◽  
Type Ii Collagen ◽  
Rankl Expression ◽  
Positive Expression ◽  
Marrow Mesenchymal Stem Cells ◽  
Bovine Type

This study analyzed the action of Bone marrow mesenchymal stem cells (BMSCs) transplantation on arthritis rat model. Arthritis rat model was established using bovine type II collagen and CFA. BMSCs phenotype was assessed by flow cytometry and pathological changes was analyzed by H&E staining along with analysis of joint severity by AI score, inflammation by ELISA as well as level of NPY, MMP-2, and MMP-9. The form of passaged BMSCs was spindle shaped with positive expression of CD29 and CD44. The structure of articular cavity in arthritis rats was disordered with infiltration of inflammatory cells which were ameliorated by BMSCs transplantation. In addition, BMSCs treatment also significantly reduced AI value, the level of VEGF, IL-17 and TNF-α as well as decreased RANK/RANKL expression and increased OPG level. In conclusion, BMSCs transplantation ameliorates inflammation and severity in arthritis rats possibly through regulation of RANK/OPG, indicating that it might be used for the treatment of arthritis patients.

scholarly journals PPAR-δ Agonist With Mesenchymal Stem Cells Induces Type II Collagen-Producing Chondrocytes in Human Arthritic Synovial Fluid

2017 ◽  
Vol 26 (8) ◽  
pp. 1405-1417 ◽  
Author(s):  
Bruce E. Heck ◽  
Joshua J. Park ◽  
Vishruti Makani ◽  
Eun-Cheol Kim ◽  
Dong Hyun Kim
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Synovial Fluid ◽  
Transforming Growth Factor ◽  
Type Ii Collagen ◽  
The United States ◽  
Synovial Inflammation ◽  
Major Constituent ◽  
Type Ii ◽  
Form Type

Osteoarthritis (OA) is an inflammatory joint disease characterized by degeneration of articular cartilage within synovial joints. An estimated 27 million Americans suffer from OA, and the population is expected to reach 67 million in the United States by 2030. Thus, it is urgent to find an effective treatment for OA. Traditional OA treatments have no disease-modifying effect, while regenerative OA therapies such as autologous chondrocyte implantation show some promise. Nonetheless, current regenerative therapies do not overcome synovial inflammation that suppresses the differentiation of mesenchymal stem cells (MSCs) to chondrocytes and the expression of type II collagen, the major constituent of functional cartilage. We discovered a synergistic combination that overcame synovial inflammation to form type II collagen-producing chondrocytes. The combination consists of peroxisome proliferator–activated receptor (PPAR) δ agonist, human bone marrow (hBM)-derived MSCs, and hyaluronic acid (HA) gel. Interestingly, those individual components showed their own strong enhancing effects on chondrogenesis. GW0742, a PPAR-δ agonist, greatly enhanced MSC chondrogenesis and the expression of type II collagen and glycosaminoglycan (GAG) in hBM-MSC-derived chondrocytes. GW0742 also increased the expression of transforming growth factor β that enhances chondrogenesis and suppresses cartilage fibrillation, ossification, and inflammation. HA gel also increased MSC chondrogenesis and GAG production. However, neither GW0742 nor HA gel could enhance the formation of type II collagen-producing chondrocytes from hBM-MSCs within human OA synovial fluid. Our data demonstrated that the combination of hBM-MSCs, PPAR-δ agonist, and HA gel significantly enhanced the formation of type II collagen-producing chondrocytes within OA synovial fluid from 3 different donors. In other words, the novel combination of PPAR-δ agonist, hBM-MSCs, and HA gel can overcome synovial inflammation to form type II collagen cartilage within human OA synovial fluid. This novel articularly injectable formula could improve OA treatment in the future clinical application.

scholarly journals The Antihypertensive Drug Nifedipine Modulates the Metabolism of Chondrocytes and Human Bone Marrow-Derived Mesenchymal Stem Cells

2019 ◽  
Author(s):  
Ilona Uzieliene ◽  
Eiva Bernotiene ◽  
Greta Urbonaite ◽  
Jaroslav Denkovskij ◽  
Edvardas Bagdonas ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Antihypertensive Drug ◽  
Mitochondrial Respiration ◽  
Collagen Type ◽  
Cell Types ◽  
Cartilage Tissue ◽  
Type Ii ◽  
Collagen Type Ii

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

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