Tenascin-C Expression in Equine Tendon-derived Cells During Proliferation and Migration

Nemoto, Manabu; Kizaki, Keiichiro; Yamamoto, Yoshio; Oonuma, Toshina; Hashizume, Kazuyoshi

doi:10.1294/jes.24.17

Cited by 15 publications

(12 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One of the tendon markers assessed was TNC , a disulfide‐linked hexamer glycoprotein and member of ECM proteoglycans (Xu et al, ) suggested to be involved in the regulation of tendon formation (Smith, Zunino, Webbon, & Heinegård, ) and repair (Nemoto, Kizaki, Yamamoto, Oonuma, & Hashizume, ). Low levels of TNC expression in tenocytes isolated from healthy adult tissue is one of the features of tensional tendon phenotype (Taylor et al, ) that combined with a high expression of COL 1 and SCX are most representative of the normal adult tendon phenotype (Taylor et al, ).…”

Section: Resultsmentioning

confidence: 99%

Human adipose tissue‐derived tenomodulin positive subpopulation of stem cells: A promising source of tendon progenitor cells

Gonçalves

Gershovich

Rodrigues

et al. 2017

J Tissue Eng Regen Med

View full text Add to dashboard Cite

Cell-based therapies are of particular interest for tendon and ligament regeneration given the low regenerative potential of these tissues. Adipose tissue is an abundant source of stem cells, which may be employed for the healing of tendon lesions. However, human adult multipotent adipose-derived stem cells (hASCs) isolated from the stromal vascular fraction of adipose tissue originate highly heterogeneous cell populations that hinder their use in specific tissue-oriented applications. In this study, distinct subpopulations of hASCs were immunomagnetic separated and their tenogenic differentiation capacity evaluated in the presence of several growth factors (GFs), namely endothelial GF, basic-fibroblast GF, transforming GF-β1 and platelet-derived GF-BB, which are well-known regulators of tendon development, growth and healing. Among the screened hASCs subpopulations, tenomodulin-positive cells were shown to be more promising for tenogenic applications and therefore this subpopulation was further studied, assessing tendon-related markers (scleraxis, tenomodulin, tenascin C and decorin) both at gene and protein level. Additionally, the ability for depositing collagen type I and III forming extracellular matrix structures were weekly assessed up to 28 days. The results obtained indicated that tenomodulin-positive cells exhibit phenotypical features of tendon progenitor cells and can be biochemically induced towards tenogenic lineage, demonstrating that this subset of hASCs can provide a reliable source of progenitor cells for therapies targeting tendon regeneration.

show abstract

Section: Resultsmentioning

confidence: 99%

Human adipose tissue‐derived tenomodulin positive subpopulation of stem cells: A promising source of tendon progenitor cells

Gonçalves

Gershovich

Rodrigues

et al. 2017

J Tissue Eng Regen Med

View full text Add to dashboard Cite

show abstract

“…All patients granted informed consent. Tendon fragments were subjected to mechanical dissociation, and maintained in Dulbecco’s Modified Eagle Medium (DMEM) containing 1% antibiotics plus 10% Fetal Bovine Serum (FBS; Nemoto et al, 2013 ); 0.25 mM L-ascorbic acid was added to the medium to allow COLVI tetramer secretion (Engvall et al, 1986 ).…”

Section: Methodsmentioning

confidence: 99%

Tendon Extracellular Matrix Alterations in Ullrich Congenital Muscular Dystrophy

Sardone

Traina

Bondi

et al. 2016

Front. Aging Neurosci.

View full text Add to dashboard Cite

Collagen VI (COLVI) is a non-fibrillar collagen expressed in skeletal muscle and most connective tissues. Mutations in COLVI genes cause two major clinical forms, Bethlem myopathy and Ullrich congenital muscular dystrophy (UCMD). In addition to congenital muscle weakness, patients affected by COLVI myopathies show axial and proximal joint contractures and distal joint hypermobility, which suggest the involvement of the tendon function. We examined a peroneal tendon biopsy and tenocyte culture of a 15-year-old patient affected by UCMD with compound heterozygous COL6A2 mutations. In patient’s tendon biopsy, we found striking morphological alterations of tendon fibrils, consisting in irregular profiles and reduced mean diameter. The organization of the pericellular matrix of tenocytes, the primary site of collagen fibril assembly, was severely affected, as determined by immunoelectron microscopy, which showed an abnormal accumulation of COLVI and altered distribution of collagen I (COLI) and fibronectin (FBN). In patient’s tenocyte culture, COLVI web formation and cell surface association were severely impaired; large aggregates of COLVI, which matched with COLI labeling, were frequently detected in the extracellular matrix. In addition, metalloproteinase MMP-2, an extracellular matrix-regulating enzyme, was increased in the conditioned medium of patient’s tenocytes, as determined by gelatin zymography and western blot. Altogether, these data indicate that COLVI deficiency may influence the organization of UCMD tendon matrix, resulting in dysfunctional fibrillogenesis. The alterations of tendon matrix may contribute to the complex pathogenesis of COLVI related myopathies.

show abstract

“…Tenocytes, the mature cell type of the tendon, have a low proliferative capacity, thus, cultured tendon cells mainly derive from progenitor cells, which display a fibroblast-like phenotype [19]. We used "tendon fibroblasts" to indicate tendon-derived cultures.…”

Section: Tendon Cell Culturesmentioning

confidence: 99%

Tendon Extracellular Matrix Remodeling and Defective Cell Polarization in the Presence of Collagen VI Mutations

Antoniel

Traina

Merlini

et al. 2020

Cells

View full text Add to dashboard Cite

Mutations in collagen VI genes cause two major clinical myopathies, Bethlem myopathy (BM) and Ullrich congenital muscular dystrophy (UCMD), and the rarer myosclerosis myopathy. In addition to congenital muscle weakness, patients affected by collagen VI-related myopathies show axial and proximal joint contractures, and distal joint hypermobility, which suggest the involvement of tendon function. To gain further insight into the role of collagen VI in human tendon structure and function, we performed ultrastructural, biochemical, and RT-PCR analysis on tendon biopsies and on cell cultures derived from two patients affected with BM and UCMD. In vitro studies revealed striking alterations in the collagen VI network, associated with disruption of the collagen VI-NG2 (Collagen VI-neural/glial antigen 2) axis and defects in cell polarization and migration. The organization of extracellular matrix (ECM) components, as regards collagens I and XII, was also affected, along with an increase in the active form of metalloproteinase 2 (MMP2). In agreement with the in vitro alterations, tendon biopsies from collagen VI-related myopathy patients displayed striking changes in collagen fibril morphology and cell death. These data point to a critical role of collagen VI in tendon matrix organization and cell behavior. The remodeling of the tendon matrix may contribute to the muscle dysfunction observed in BM and UCMD patients.

show abstract

Tenascin-C Expression in Equine Tendon-derived Cells During Proliferation and Migration

Cited by 15 publications

References 28 publications

Human adipose tissue‐derived tenomodulin positive subpopulation of stem cells: A promising source of tendon progenitor cells

Human adipose tissue‐derived tenomodulin positive subpopulation of stem cells: A promising source of tendon progenitor cells

Tendon Extracellular Matrix Alterations in Ullrich Congenital Muscular Dystrophy

Tendon Extracellular Matrix Remodeling and Defective Cell Polarization in the Presence of Collagen VI Mutations

Contact Info

Product

Resources

About