Periostin expression distinguishes between light and dark hypertrophic chondrocytes

Chen, Kuan-Sheng; Tatarczuch, Liliana; Mirams, Michiko; Ahmed, Youssef; Pagel, Charles N.; Mackie, Eleanor J.

doi:10.1016/j.biocel.2010.01.018

Cited by 17 publications

(14 citation statements)

References 17 publications

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“…It is well known that hypertrophy and nonapoptotic physiological cell death of chondrocytes are vital processes of endochondral ossification [15, 16]; therefore, we suppose that this pathological alteration is a major response in the spinal deformity of KO mice.…”

Section: Resultsmentioning

confidence: 98%

Chondrocyte-Specific Knockout of TSC-1 Leads to Congenital Spinal Deformity in Mice

Yang

Chen

et al. 2017

BioMed Research International

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Congenital spinal deformity is the most severe clinical orthopedic issue worldwide. Among all the pathological processes of congenital spinal deformity, the imbalance of endochondral ossification is considered to be the most important developmental cause of spinal dysplasia. We established chondrocyte-specific TSC-1 knockout (KO) mice to overactivate the energy metabolic component, mammalian target of rapamycin complex 1 (mTORC1), and measured the spinal development by general, imaging, histological, and Western-blot assessments. In addition to skeletal dysplasia, the KO mice displayed severe congenital spinal deformity and significant intervertebral disc changes. This study suggests that, in the process of endochondral ossification, excessive activation of mTORC1 signaling in chondrocytes induces obvious spinal deformity, and the chondrocytes may be the cell type responsible for congenital spinal deformity.

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Section: Resultsmentioning

confidence: 98%

Chondrocyte-Specific Knockout of TSC-1 Leads to Congenital Spinal Deformity in Mice

Yang

Chen

et al. 2017

BioMed Research International

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“…Another study reported expression of the periostin-like factor, a splice variant of periostin, in tenocytes of trained but not of untrained tendon tissue [22]. In addition, one study observed periostin expression in a subset of hypertrophic chondrocytes of the growth plate [23].…”

Section: Discussionmentioning

confidence: 97%

Periostin Secreted by Mesenchymal Stem Cells Supports Tendon Formation in an Ectopic Mouse Model

Noack

Seiffart

Willbold

et al. 2014

Stem Cells and Development

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True tendon regeneration in human patients remains a vision of musculoskeletal therapies. In comparison to other mesenchymal lineages the biology of tenogenic differentiation is barely understood. Specifically, easy and efficient protocols are lacking that might enable tendon cell and tissue differentiation based on adult (stem) cell sources. In the murine mesenchymal progenitor cell line C3H10T½, overexpression of the growth factor bone morphogenetic protein 2 (BMP2) and a constitutively active transcription factor, Smad8 L + MH2, mediates tendon cell differentiation in vitro and the formation of tendon-like tissue in vivo. We hypothesized that during this differentiation secreted factors involved in extracellular matrix formation exert a major impact on tendon development. Gene expression analyses revealed four genes encoding secreted factors that are notably upregulated: periostin, C-type lectin domain family 3 (member b), RNase A4, and follistatin-like 1. These factors have not previously been implicated in tendon biology. Among these, periostin showed a specific expression in tenocytes of adult mouse Achilles tendon and in chondrocytes within the nonmineralized fibrocartilage zone of the enthesis with the calcaneus. Overexpression of periostin alone or in combination with constitutively active BMP receptor type in human mesenchymal stem cells and subsequent implantation into ectopic sites in mice demonstrated a reproducible moderate tenogenic capacity that has not been described before. Therefore, periostin may belong to the factors contributing to the development of tenogenic tissue.

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“…3; Anderson 1964, Hwang 1978, Wilsman et al 1981, Roach & Clarke 2000, Ahmed et al 2007. The fact that these two populations could only be identified by electron microscopy has made it difficult to study their functional differences, but the recent identification of periostin as a dark chondrocyte-associated protein will assist in research in this area (Chen et al 2010).…”

Section: Hypertrophymentioning

confidence: 99%

The skeleton: a multi-functional complex organ. The growth plate chondrocyte and endochondral ossification

Mackie¹,

Tatarczuch²,

Mirams³

2011

Journal of Endocrinology

368

319

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Endochondral ossification is the process that results in both the replacement of the embryonic cartilaginous skeleton during organogenesis and the growth of long bones until adult height is achieved. Chondrocytes play a central role in this process, contributing to longitudinal growth through a combination of proliferation, extracellular matrix (ECM) secretion and hypertrophy. Terminally differentiated hypertrophic chondrocytes then die, allowing the invasion of a mixture of cells that collectively replace the cartilage tissue with bone tissue. The behaviour of growth plate chondrocytes is tightly regulated at all stages of endochondral ossification by a complex network of interactions between circulating hormones (including GH and thyroid hormone), locally produced growth factors (including Indian hedgehog, WNTs, bone morphogenetic proteins and fibroblast growth factors) and the components of the ECM secreted by the chondrocytes (including collagens, proteoglycans, thrombospondins and matrilins). In turn, chondrocytes secrete factors that regulate the behaviour of the invading bone cells, including vascular endothelial growth factor and receptor activator of NFkB ligand. This review discusses how the growth plate chondrocyte contributes to endochondral ossification, with some emphasis on recent advances.

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Periostin expression distinguishes between light and dark hypertrophic chondrocytes

Cited by 17 publications

References 17 publications

Chondrocyte-Specific Knockout of TSC-1 Leads to Congenital Spinal Deformity in Mice

Chondrocyte-Specific Knockout of TSC-1 Leads to Congenital Spinal Deformity in Mice

Periostin Secreted by Mesenchymal Stem Cells Supports Tendon Formation in an Ectopic Mouse Model

The skeleton: a multi-functional complex organ. The growth plate chondrocyte and endochondral ossification

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