Introduction
This page describes skeletal tendon development, during formation of the connective tissue connection muscle to bone.
The syndetome is the embryonic structural origin of tendons from the somite and originates from the dorsolateral edge of the sclerotome. Expression of the basic helix-loop-helix (bHLH) transcription factor scleraxis (SCX) in early progenitor cells is thought to be key regulator in the formation of tendon and ligament tissues.[1] Scleraxis may also have additional roles in other tissues such as in early heart valve development.[2]
The origins of some muscles and tendons in the head differ from those found in the remained of the body.
See also notes Connective Tissue Development.
Some Recent Findings
- Cellular and molecular maturation in fetal and adult ovine calcaneal tendons [3] "ovine tendon morphology undergoes profound transformations during this period. Endotenon was more developed in fetal tendons than in adult tissues, and its cell phenotype changed through tendon maturation. Indeed, groups of large rounded cells laying on smaller and more compacted ones expressing osteocalcin, vascular endothelial growth factor (VEGF) and nerve growth factor (NGF) were identified exclusively in fetal mid-stage tissues, and not in late fetal or adult tendons. VEGF, NGF as well as blood vessels and nerve fibers showed decreased expression during tendon development. Moreover, the endotenon of mid- and late fetuses contained identifiable cells that expressed several pluripotent stem cell markers [Telomerase Reverse Transcriptase (TERT), SRY Determining Region Y Box-2 (SOX2), Nanog Homeobox (NANOG) and Octamer Binding Transcription Factor-4A (OCT-4A)]. These cells were not identifiable in adult specimens. Ovine tendon development was also accompanied by morphological modifications to cell nuclei, and a progressive decrease in cellularity, proliferation index and expression of connexins 43 and 32. Tendon maturation was similarly characterised by modulation of several other gene expression profiles, including Collagen type I, Collagen type III, Scleraxis B, Tenomodulin, Trombospondin 4 and Osteocalcin. These gene profiles underwent a dramatic reduction in adult tissues. Transforming growth factor-β~1 expression (involved in collagen synthesis) underwent a similar decrease."
- Embryonic mechanical and soluble cues regulate tendon progenitor cell gene expression as a function of developmental stage and anatomical origin.[4] "Stem cell-based engineering strategies for tendons have yet to yield a normal functional tissue, due in part to a need for tenogenic factors. Additionally, the ability to evaluate differentiation has been challenged by a lack of markers for differentiation.... Based on scleraxis expression, TGFβ2 was tenogenic for TPCs at all stages, while loading was for late-stage cells only, and FGF4 had no effect despite regulation of other genes. When factors were combined, TGFβ2 continued to be tenogenic, while FGF4 appeared anti-tenogenic. Various treatments elicited distinct responses by axial vs. limb TPCs of specific stages. These results identified tenogenic factors, suggest tendon engineering strategies should be customized for tissues by anatomical origin, and provide stage-specific gene expression profiles of limb and axial TPCs as benchmarks with which to monitor tenogenic differentiation of stem cells."
- Connecting muscles to tendons: tendons and musculoskeletal development in flies and vertebrates[5] "The formation of the musculoskeletal system represents an intricate process of tissue assembly involving heterotypic inductive interactions between tendons, muscles and cartilage. An essential component of all musculoskeletal systems is the anchoring of the force-generating muscles to the solid support of the organism: the skeleton in vertebrates and the exoskeleton in invertebrates. Here, we discuss recent findings that illuminate musculoskeletal assembly in the vertebrate embryo, findings that emphasize the reciprocal interactions between the forming tendons, muscle and cartilage tissues. We also compare these events with those of the corresponding system in the Drosophila embryo, highlighting distinct and common pathways that promote efficient locomotion while preserving the form of the organism."
- Slowdown promotes muscle integrity by modulating integrin-mediated adhesion at the myotendinous junction [6]
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More recent papers
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Molecular
Mesoderm Development and Pax[7]
dark green - syndetome originates from the dorsolateral edge of the sclerotome, as Pax1 and Pax9 are downregulated and scleraxis (Scx) upregulation leads to syndegenesis. Pax, paired homeobox; MYOD1, myogenic differentiation antigen 1; MYF5, myogenic factor 5; NKX, NK homeobox; SCX, scleraxis.
Scleraxis
Scleraxis (SCX) is a member of the basic helix-loop-helix (bHLH) transcription factor family. It is expressed in early mesoderm progenitor cells and may regulate the formation of tendon and ligament tissues.[1]
Scleraxis may also have additional roles in other tissues such as in early heart valve development.[2]
- Cytogenetic location: 8q24.3
- Links: NCBI databases - Scleraxis | OMIM 609067
Tenomodulin
Tenomodulin is a marker of tendon differentiation, its expression has been shown to be regulated by the transcription factors Scleraxis and Mohawk.[8]
- Links: NCBI databases - Tenomodulin
Histology
References
- ↑ 1.0 1.1 <pubmed>11585810</pubmed>
- ↑ 2.0 2.1 <pubmed>24983472</pubmed>
- ↑ <pubmed>25546075</pubmed>
- ↑ <pubmed>24231248</pubmed>
- ↑ <pubmed>20699295</pubmed>
- ↑ <pubmed>20110313</pubmed>
- ↑ <pubmed>24496612</pubmed>| Development
- ↑ <pubmed>24834008</pubmed>
Reviews
Articles
<pubmed>12705871</pubmed>
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Cite this page: Hill, M.A. (2024, April 26) Embryology Musculoskeletal System - Tendon Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Musculoskeletal_System_-_Tendon_Development
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- © Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G