Expression of the TGF-β/BMP inhibitor EVI1 in human dental pulp cells

Durand, Simon; Roméas, Annick; Couble, Marie‐Lise; Langlois, Dominique; Li, Jacques Y.; Magloire, H.; Bleicher, Françoise; Staquet, Marie‐Jeanne; Farges, Jean‐Christophe

doi:10.1016/j.archoralbio.2007.01.012

Cited by 8 publications

(4 citation statements)

References 38 publications

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“…TGF‐β receptors I and II are expressed in odontoblasts and pulp cells, with more homogenous expression in carious teeth due to increased expression in the underlying pulp cell population, including blood vessel‐associated cells . However, TGF‐β/BMP inhibitor EVI‐1 (ecotropic viral integration site‐1) is present in pulp core cells and subodontoblastic cells, but is almost absent in coronal odontoblasts . TGF‐β1 can induce apoptosis in various cell types including odontoblast‐like cells in vitro .…”

Section: Growth Factors In Dentinmentioning

confidence: 99%

A review of the nature, role, and function of dentin non‐collagenous proteins. Part II: enzymes, serum proteins, and growth factors

Mazzoni¹,

Breschi²,

Carrilho³

et al. 2009

Endodontic Topics

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Part I was an overview of the role and function of proteoglycans and glycoproteins in the pulpo–dentin complex; part II will focus on enzymes, serum proteins, and growth factors. This review will discuss current knowledge regarding matrix metalloproteinases (MMPs), cathepsins, serum proteins, and growth factors in dentin and the related dentin–pulp complex in an attempt to better understand their nature, role, and function in the dentin extracellular matrix (ECM) environment. Dentin formation in physiological and pathological conditions has been widely studied. However, the regulation and involvement of non‐collageneous enzymes, serum proteins, and growth factors are still not completely elucidated. MMPs, a family of 23 endopeptidases in humans, are collectively capable of degrading virtually all ECM components, and their specific tissue inhibitors (TIMPs: tissue inhibitors of matrix metalloproteinases) participate in organo‐ and morphogenesis, physiological tissue turnover, and pathological tissue destruction. Similarly, the lysosomal cysteine proteinases (cathepsins) are capable of degrading ECM proteins such as collagen, laminin, fibronectin, and proteoglycans. These enzymes are implicated in a variety of pathological conditions, especially in diseases involving tissue re‐modeling states. Dentin also contains serum‐derived proteins (such as albumin, immunoglobulins, and transferrin), and a variety of growth factors in the mineralized ECM are available for release during demineralization or other injury. A detailed description of the components of the above‐mentioned dentin non‐collageneous proteins will be summarized in this literature review.

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Section: Growth Factors In Dentinmentioning

confidence: 99%

A review of the nature, role, and function of dentin non‐collagenous proteins. Part II: enzymes, serum proteins, and growth factors

Mazzoni¹,

Breschi²,

Carrilho³

et al. 2009

Endodontic Topics

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“…For example, nuclear factor I‐C regulates dentin sialophosphoprotein (DSPP) and E‐cadherin by control of Kruppel‐like factor 4 during dentinofenesis. The TGF‐beta/BMP family of growth factors induce odontoblast differentiation and reparative dentin synthesis . HMGB1 promotes proliferation and differentiation of human DPCs.…”

Section: Introductionmentioning

confidence: 99%

Effects of neurotrophin receptor‐mediated MAGE homology on proliferation and odontoblastic differentiation of mouse dental pulp cells

et al. 2015

Cell Proliferation

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“…For example, P300 and CREB-binding protein interactions with Smads can increase the transcription of target genes by making the transcriptional machinery more accessible (53). However, transcriptional co-repressors, including Ski and Ski related novel gene, ecotropic viral integration site-1, TG interacting factor (TGIF)1 and TGIF2, prevent Smad 3/4 from binding to the SBE of BMP-responsive genes (54)(55)(56)(57). Lastly, the BMP pathway can be influenced by Smad ubiquitination regulatory factor (Smurf)1/2, which induce degradation of Smads (Fig.…”

Section: Signal Transduction Of Bmpmentioning

confidence: 99%

Bone morphogenetic proteins mediate crosstalk between cancer cells and the tumour microenvironment at primary tumours and metastases (Review)

et al. 2020

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Bone morphogenetic proteins (BMP) are pluripotent molecules, co-ordinating cellular functions from early embryonic and postnatal development to tissue repair, regeneration and homeostasis. They are also involved in tumourigenesis, disease progression and the metastasis of various solid tumours. Emerging evidence has indicated that BMPs are able to promote disease progression and metastasis by orchestrating communication between cancer cells and the surrounding microenvironment. The interactions occur between BMPs and epidermal growth factor receptor, hepatocyte growth factor, fibroblast growth factor, vascular endothelial growth factor and extracellular matrix components. Overall, these interactions co-ordinate the cellular functions of tumour cells and other types of cell in the tumour to promote the growth of the primary tumour, local invasion, angiogenesis and metastasis, and the establishment and survival of cancer cells in the metastatic niche. Therefore, the present study aimed to provide an informative summary of the involvement of BMPs in the tumour microenvironment.

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Expression of the TGF-β/BMP inhibitor EVI1 in human dental pulp cells

Cited by 8 publications

References 38 publications

A review of the nature, role, and function of dentin non‐collagenous proteins. Part II: enzymes, serum proteins, and growth factors

A review of the nature, role, and function of dentin non‐collagenous proteins. Part II: enzymes, serum proteins, and growth factors

Effects of neurotrophin receptor‐mediated MAGE homology on proliferation and odontoblastic differentiation of mouse dental pulp cells

Bone morphogenetic proteins mediate crosstalk between cancer cells and the tumour microenvironment at primary tumours and metastases (Review)

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