ArticleBone2012
MEPE is a novel regulator of growth plate cartilage mineralization.
Article in Bone, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- Knockdown of MEPE Promotes Cranial Defect Repair and Activates the cAMP/PKA Signaling Pathway.Biochemical genetics · 2026Article
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- The Ex Vivo Organ Culture of Bone and Cartilage.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Article
- Tenascin-C is a driver of inflammation in the DSS model of colitis.Matrix biology plus · 2022Article
- Cellular and Molecular Alterations Underlying Abnormal Bone Growth in X-Linked Hypophosphatemia.International journal of molecular sciences · 2022Review
- Matricellular proteins in cutaneous wound healing.Frontiers in cell and developmental biology · 2022Review
- A Rare Cause of Hypophosphatemia: Raine Syndrome Changing Clinical Features with Age.Calcified tissue international · 2020Article
- The STR/ort mouse model of spontaneous osteoarthritis - an update.Osteoarthritis and cartilage · 2017Review
- Culture of Murine Embryonic Metatarsals: A Physiological Model of Endochondral Ossification.Journal of visualized experiments : JoVE · 2016Article
- E11/Podoplanin Protein Stabilization Through Inhibition of the Proteasome Promotes Osteocyte Differentiation in Murine in Vitro Models.Journal of cellular physiology · 2016Article
- Endochondral Growth Defect and Deployment of Transient Chondrocyte Behaviors Underlie Osteoarthritis Onset in a Natural Murine Model.Arthritis & rheumatology (Hoboken, N.J.) · 2016Article
- MEPE Localization in the Craniofacial Complex and Function in Tooth Dentin Formation.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2016Article
- Models of ex vivo explant cultures: applications in bone research.BoneKEy reports · 2016Article
- Expression of Sulf1 and Sulf2 in cartilage, bone and endochondral fracture healing.Histochemistry and cell biology · 2016Article
- The Functional co-operativity of Tissue-Nonspecific Alkaline Phosphatase (TNAP) and PHOSPHO1 during initiation of Skeletal Mineralization.Biochemistry and biophysics reports · 2015Article
- Increased linear bone growth by GH in the absence of SOCS2 is independent of IGF-1.Journal of cellular physiology · 2015Article
- Article
- An in situ hybridization study of perlecan, DMP1, and MEPE in developing condylar cartilage of the fetal mouse mandible and limb bud cartilage.European journal of histochemistry : EJH · 2015Article
- Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Matrix extracellular phosphoglycoprotein (MEPE) belongs to the SIBLING protein family which play key roles in biomineralization. Although the growth plates of MEPE-overexpressing mice display severe morphological disruption, the expression and function of MEPE in growth plate matrix mineralization remains largely undefined. Here we show MEPE and its cleavage product, the acidic serine aspartate-rich MEPE-associated motif (ASARM) peptide, to be localised to the hypertrophic zone of the growth plate. We also demonstrate that the phosphorylated (p)ASARM peptide inhibits ATDC5 chondrocyte matrix mineralization. Stable MEPE-overexpressing ATDC5 cells also had significantly reduced matrix mineralization in comparison to the control cells. Interestingly, we show that the addition of the non-phosphorylated (np)ASARM peptide promoted mineralization in the ATDC5 cells. The peptides and the overexpression of MEPE did not affect the differentiation of the ATDC5 cells. For a more physiologically relevant model, we utilized the metatarsal organ culture model. We show the pASARM peptide to inhibit mineralization at two stages of development, as shown by histological and μCT analysis. Like in the ATDC5 cells, the peptides did not affect the differentiation of the metatarsals indicating that the effects seen on mineralization are direct, as is additionally confirmed by no change in alkaline phosphatase activity or mRNA expression. In the metatarsal organ cultures, the pASARM peptide also reduced endothelial cell markers and vascular endothelial growth factor mRNA expression. Taken together these results show MEPE to be an important regulator of growth plate chondrocyte matrix mineralization through its cleavage to an ASARM peptide.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.