Intrinsic differentiation potential of adolescent human tendon tissue: an in-vitro cell differentiation study

Mos, Marieke de; Koevoet, Wendy; Jahr, Holger; Verstegen, Monique M A; Heijboer, M.P.; Kops, Nicole; Leeuwen, Johannes P.T.M. van; Weinans, Harrie; Verhaar, Jan A N; Osch, Gerjo J. V. M. van

doi:10.1186/1471-2474-8-16

Cited by 96 publications

(85 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ectopic bone formation in the Achilles tendon after mid-point tenotomy has also been reported to be caused by the direct conversion of tendon tissue to cartilage (Rooney et al, 1993). Other studies also reported the presence of resident progenitor cells with multidifferentiation potential in the tendon (Salingcarnboriboon et al 2003;Bi et al 2007;de Mos et al 2007). Injection of recombinant human bone morphogenetic protein -2 (rhBMP-2) into the tendon increased ectopic bone formation, indicating that the tendon consisted of cells that were responsive to BMP and were capable of differentiating along the chondro-osseous pathway (Hashimoto et al 2007).…”

Section: Discussionmentioning

confidence: 95%

“…Recent studies reported that human and mouse tendons harbored a unique cell population with universal stem cell characteristics (tendon stem/progenitor cells), and they could differentiate into chondrocytes and osteoblasts (Salingcarnboriboon et al 2003;Bi et al 2007;de Mos et al 2007). These isolated tendon stem/progenitor cells could regenerate tendon-like tissues after extended expansion in vitro and transplantation in vivo (Bi et al 2007).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Chondrocyte Phenotype and Ectopic Ossification in Collagenase-induced Tendon Degeneration

Lui

Chan

et al. 2008

J Histochem Cytochem.

103

View full text Add to dashboard Cite

S U M M A R Y We report chondrocyte phenotype and ectopic ossification in a collagenaseinduced patellar tendon injury model. Collagenase or saline was injected intratendinously in one limb. The patella tendon was harvested for assessment at different times. There was an increase in cellularity, vascularity, and loss of matrix organization with time after collagenase injection. The tendon did not heal histologically until week 32. Ectopic mineralization as indicated by von Kossa staining started from week 8. Tendon calcification was mediated by endochondral ossification, as shown by expression of type X collagen. viva CT imaging and polarization microscopy showed characteristic bony porous structures and collagen fiber arrangement, respectively, in the calcific regions. Marrow-like cells and blood vessels were observed inside calcific deposits. Chondrocyte-like cells as indicated by morphology, expression of type II collagen, and sox 9 were seen around and embedded inside the calcific deposits. Fibroblast-like cells expressed type II collagen and sox 9 at earlier times, suggesting that erroneous differentiation of healing tendon fibroblasts may account for failed healing and ossification in collagenase-induced tendon degeneration. Because this animal model replicates key histopathological changes in calcific tendinopathy, it can be used as a model for the study of its pathogenesis at the patellar tendon.

show abstract

Section: Discussionmentioning

confidence: 95%

mentioning

confidence: 99%

Chondrocyte Phenotype and Ectopic Ossification in Collagenase-induced Tendon Degeneration

Lui

Chan

et al. 2008

J Histochem Cytochem.

103

View full text Add to dashboard Cite

show abstract

“…Primers were designed using PrimerExpress 2.0 software (Applied Biosystems, Foster City, CA) to meet SYBR 1 Green (TLRs only) or Taqman 1 requirements. BLASTn ensured gene specificity of the following primers: TLR2 (F: 5 0 -CTACTGGGTGGAGAACCTTATGGT-3 0 ; R: 5 0 -CCGCTTATGAAGACACAACTTGA-3 0 ), TLR4 (F: 5 0 -GGCATGCCTGTGCTGAGTT-3 0 ; R: 5 0 -CTGCTACAACAGA-TACTACAAGCACACT-3 0 ), MMP1, MMP3, MMP9, MMP13, 7 and GAPDH 13 as calibrator. For real-time RT-PCR 20 mL samples were prepared containing sample cDNA, forward and reverse primers, and either qPCR TM Mastermix Plus for SYBR 1 Green I (Eurogentec, Nederland B.V., Maastricht, The Netherlands) or TaqMan 1 Universal PCR MasterMix (ABI, Branchburg, NJ), according to the manufacturer's guidelines.…”

Section: Rna Isolation and Real-time Rt-pcrmentioning

confidence: 99%

Tendon degeneration is not mediated by regulation of Toll‐like receptors 2 and 4 in human tenocytes

Mos

Joosten

Oppers‐Walgreen

et al. 2009

Journal Orthopaedic Research

Self Cite

View full text Add to dashboard Cite

We hypothesized that expression of Toll-like receptors (TLRs) 2 and 4 by tenocytes is involved in the catabolic processes of tendon degeneration. We investigated TLR2 and TLR4 expression by tenocytes in healthy and tendinotic Achilles tendons. We also investigated whether TLR2 and TLR4 could be upregulated in tendon explants using proinflammatory cytokines interleukin (IL)-1b and tumor necrosis factor alphpa (TNFa). Peroperatively harvested healthy (n ¼ 5) and tendinotic (n ¼ 13) Achilles tendon samples were examined by real-time RT-PCR and immunohistochemical staining for TLR2 and TLR4. In addition, the catabolic process in tendinopathy was analyzed by real-time RT-PCR for matrix metalloproteinases MMP1, MMP3, MMP9, and MMP13. Furthermore, healthy tendon explants were cultured in the presence of 20 ng/ml IL-1b (n ¼ 10) or 10 ng/mL TNFa (n ¼ 8) for 4, 24, 48, and 72 h before analysis of TLR and MMP expression levels. Although mRNA levels for both TLR2 and TLR4 were detected in healthy and tendinotic Achilles tendons, we could not confirm expression of these receptors by immunohistochemical staining in either healthy or tendinotic tendon samples. Both receptors did not show significant transcriptional regulation in tendinopathy, although MMP3 was downregulated and MMP9 was upregulated in tendinopathy. In tendon explant cultures TLR2 mRNA was upregulated by TNFa (p < 0.05) and IL-1b (not significant). TLR4 gene expression was not altered by addition of IL-1b or TNFa. Tendon tissue can be stimulated to increase TLR2 gene expression by addition of catabolic factors TNFa or IL-1b. However, the catabolic processes in Achilles tendinopathy cannot be attributed to regulation of TLR2 and TLR4 by tenocytes. Toll-like receptors (TLRs) are phylogenetically conserved transmembrane receptors belonging to the family of pattern-recognition receptors (PRR). In humans, 11 TLR homologs have been identified thus far, expressed by numerous cell types like monocytes and dendritic cells, 1 and for example by chondrocytes. 2 TLRs detect microbial components, but TLR2 and TLR4 also recognize endogenous ligands like heat-shock proteins, necrotic cells, hyaluronan, and fibronectin. 1 Ligand recognition elicits an immune response with upregulation and activation of proinflammatory cytokines and matrix-metalloproteinases (MMPs). 2 Hence, via endogenous ligand recognition the TLR-mediated catabolic signalling pathways can directly contribute to degradative tissue reactions even in the absence of microbial components. TLRs are implicated in inflammatory and autoimmune diseases, but also in disorders like atherosclerosis and cancer. 3,4 Furthermore they play a role in noninfected rheumatoid arthritis (RA) and in the primarily degenerative joint disease osteoarthritis (OA). [1][2][3]5,6 In degenerative tendinopathies the balance between matrix synthesis and degradation is disturbed, and increased MMP activity as well as an increased percentage of degraded collagen are found. 7-9 An increase in NO synthase expression was found in a sup...

show abstract

“…Clinically speaking this would not be a desired outcome and should be avoided, in the same way that miss-expression and differentiation down an inappropriate path could compromise the native tissue properties. Therefore, it would be essential to standardize any genetic modification of cells (although difficult) to limit MSCs sending inappropriate signals to the environment, as has been demonstrated in the laboratory [5].…”

Section: Basic Scientific Researchmentioning

confidence: 99%

“…As the animal grows, cells develop into different types of connective tissue; bone, tendon, cartilage, the lymphatic and circulatory systems [3,4] http://en.wikipedia.org/wiki/Mesenchymecite_note-isbn0-7817-8577-4-2. These cells thrive and survive within the collagen based matrix, which provides feedback to the cells based on architectural configuration, thought to influence certain activity in response to chemical stimuli [5]. As embryology progresses subsets of the mesenchyme will give rise to the bone and cartilaginous framework of the organism as well as the ligaments and tendons which make up the 'soft tissue skeleton'.…”

mentioning

confidence: 99%

Current Issues and Regulations in Tendon Regeneration and Musculoskeletal Repair with Mesenchymal Stem Cells

Grange¹

2012

CSCR

View full text Add to dashboard Cite

Intrinsic differentiation potential of adolescent human tendon tissue: an in-vitro cell differentiation study

Cited by 96 publications

References 41 publications

Chondrocyte Phenotype and Ectopic Ossification in Collagenase-induced Tendon Degeneration

Chondrocyte Phenotype and Ectopic Ossification in Collagenase-induced Tendon Degeneration

Tendon degeneration is not mediated by regulation of Toll‐like receptors 2 and 4 in human tenocytes

Current Issues and Regulations in Tendon Regeneration and Musculoskeletal Repair with Mesenchymal Stem Cells

Contact Info

Product

Resources

About