Extracellular matrix derived from chondrocytes promotes rapid expansion of human primary chondrocytes in vitro with reduced dedifferentiation

Mao, Yong; Block, Travis J.; Singh-Varma, Anya; Sheldrake, Anne; Leeth, Rachel A.; Griffey, Sy; Kohn, Joachim

doi:10.1016/j.actbio.2018.12.006

Cited by 38 publications

(47 citation statements)

References 52 publications

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“…HESR dishes functionalized with a cartilage extract were more effective at inhibiting chondrocytic dedifferentiation than control dishes. Another group further developed biomimetic materials using decellularized ECM derived from human articular chondrocytes 14 . These biomaterials were more effective at maintaining the phenotype and enhancing the proliferation of chondrocytes than standard culture plates.…”

Section: Dedifferentiation In Diseases (As a Pathological Factor)mentioning

confidence: 99%

“…In addition, some specific biomolecules trigger the dedifferentiation of vascular smooth muscle cells 12 or chondrocytes 13 via the mitogen-activated protein kinase (MAPK) pathways. Also, innovative biomaterials are designing and creating to regulate dedifferentiation 14 , 15 . As our understanding of the molecular mechanisms of dedifferentiation improves, therapeutic methods using dedifferentiation present tremendous potential.…”

Section: Introductionmentioning

confidence: 99%

“…npj Regenerative Medicine (2020)14 Published in partnership with the Australian Regenerative Medicine Institute…”

mentioning

confidence: 99%

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Dedifferentiation: inspiration for devising engineering strategies for regenerative medicine

Yao

Wang

2020

npj Regen Med

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Cell dedifferentiation is the process by which cells grow reversely from a partially or terminally differentiated stage to a less differentiated stage within their own lineage. This extraordinary phenomenon, observed in many physiological processes, inspires the possibility of developing new therapeutic approaches to regenerate damaged tissue and organs. Meanwhile, studies also indicate that dedifferentiation can cause pathological changes. In this review, we compile the literature describing recent advances in research on dedifferentiation, with an emphasis on tissue-specific findings, cellular mechanisms, and potential therapeutic applications from an engineering perspective. A critical understanding of such knowledge may provide fresh insights for designing new therapeutic strategies for regenerative medicine based on the principle of cell dedifferentiation.

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Section: Dedifferentiation In Diseases (As a Pathological Factor)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Dedifferentiation: inspiration for devising engineering strategies for regenerative medicine

Yao

Wang

2020

npj Regen Med

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“…Therefore, hypersecretion of these proteases by chondrocytes may result in an increased degradation of cartilaginous ECM and compromised cartilage homeostasis in Gnptg-deficient mice. Cartilage possesses limited self-regenerative capacity, and the efficiency of cartilage repair depends on the composition and structure of ECM, which delivers specific biological signals to the embedded chondrocytes (Emans and Peterson, 2014;Mao et al, 2019). Hence, even minor changes in the cartilage ECM may affect chondrocyte differentiation and provide a positive feedback which aggravates cartilage dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Imbalanced cellular metabolism compromises cartilage homeostasis and joint function in a mouse model of mucolipidosis type III gamma

Westermann

Fleischhauer

Vogel³

et al. 2020

Disease Models &Amp; Mechanisms

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Mucolipidosis type III (MLIII) gamma is a rare inherited lysosomal storage disorder caused by mutations in GNPTG encoding the γ-subunit of GlcNAc-1-phosphotransferase, the key enzyme ensuring proper intracellular location of multiple lysosomal enzymes. Patients with MLIII gamma typically present with osteoarthritis and joint stiffness, suggesting cartilage involvement. Using Gnptgko mice as a model of the human disease, we showed that missorting of a number of lysosomal enzymes is associated with intracellular accumulation of chondroitin sulfate in Gnptgkochondrocytes and their impaired differentiation, as well as with an altered microstructure of the cartilage extracellular matrix (ECM). We also demonstrated distinct functional and structural properties of the Achilles tendons isolated from Gnptgko and Gnptabki mice, the latter displaying a more severe phenotype resembling mucolipidosis type II (MLII) in humans. Together with comparative analyses of joint mobility in MLII and MLIII patients, these findings provide a basis for better understanding of the molecular reasons leading to joint pathology in these patients. Our data suggest that lack of GlcNAc-1-phosphotransferase activity due to defects in the γ-subunit causes structural changes within the ECM of connective and mechanosensitive tissues, such as cartilage and tendon, and eventually results in functional joint abnormalities typically observed in MLIII gamma patients. This idea was supported by a deficit of the limb motor function in Gnptgko mice challenged on a Rotarod under fatigue-associated conditions, suggesting that the impaired motor performance of Gnptgko mice was caused by fatigue and/or pain at the joint.

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“…65 To overcome the unfavourable microenvironment of a cartilage defect, Mao and colleagues used ECM derived from allogeneic human articular chondrocytes, which promoted the expansion of human primary chondrocytes in vitro with reduced dedifferentiation. 51 Second, products from platelets promote cartilage repair following costal cartilage grafting. A hybrid technique involving the implantation of hyaline cartilage chips, platelet-poor plasma and intra-articular injection of growth-factor-rich plasma, enhanced chondrogenesis and yielded hyaline cartilage in a sheep model.…”

Section: Costal Chondral/osteochondral Grafting In Animal Modelsmentioning

confidence: 99%

Autologous costal chondral transplantation and costa-derived chondrocyte implantation: emerging surgical techniques

Gao

et al. 2019

Therapeutic Advances in Musculoskeletal

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It is a great challenge to cure symptomatic lesions and considerable defects of hyaline cartilage due to its complex structure and poor self-repair capacity. If left untreated, unmatured degeneration will cause significant complications. Surgical intervention to repair cartilage may prevent progressive joint degeneration. A series of surgical techniques, including biological augmentation, microfracture and bone marrow stimulation, autologous chondrocyte implantation (ACI), and allogenic and autogenic chondral/osteochondral transplantation, have been used for various indications. However, the limited repairing capacity and the potential pitfalls of these techniques cannot be ignored. Increasing evidence has shown promising outcomes from ACI and cartilage transplantation. Nevertheless, the morbidity of autologous donor sites and limited resource of allogeneic bone have considerably restricted the wide application of these surgical techniques. Costal cartilage, which preserves permanent chondrocytes and the natural osteochondral junction, is an ideal candidate for the restoration of cartilage defects. Several in vitro and in vivo studies have shown good performance of costal cartilage transplantation. Although costal cartilage is a classic donor in plastic and cosmetic surgery, it is rarely used in skeletal cartilage restoration. In this review, we introduce the fundamental properties of costal cartilage and summarize costa-derived chondrocyte implantation and costal chondral/osteochondral transplantation. We will also discuss the pitfalls and pearls of costal cartilage transplantation. Costal chondral/osteochondral transplantation and costa-based chondrocytotherapy might be up-and-coming surgical techniques for recalcitrant cartilage lesions.

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Extracellular matrix derived from chondrocytes promotes rapid expansion of human primary chondrocytes in vitro with reduced dedifferentiation

Cited by 38 publications

References 52 publications

Dedifferentiation: inspiration for devising engineering strategies for regenerative medicine

Dedifferentiation: inspiration for devising engineering strategies for regenerative medicine

Imbalanced cellular metabolism compromises cartilage homeostasis and joint function in a mouse model of mucolipidosis type III gamma

Autologous costal chondral transplantation and costa-derived chondrocyte implantation: emerging surgical techniques

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