Evidence map›Paper›PMID 23629661›Full record

ArticleThe Journal of biological chemistry2013

Myocilin stimulates osteogenic differentiation of mesenchymal stem cells through mitogen-activated protein kinase signaling.

Heung Sun Kwon, Thomas V Johnson, Stanislav I Tomarev

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.6field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  5. International journal of molecular sciences · 2023
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  15. Targeting P38 Pathway Regulates Bony FormationInternational journal of medical sciences · 2016
    Article
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  18. Article
  19. CaMKII plays a part in the chondrogenesis of bone marrow-derived mesenchymal stem cells.International journal of clinical and experimental pathology · 2015
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Heung Sun KwonSection of Retinal Ganglion Cell Biology, Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892.
Thomas V JohnsonSection of Retinal Ganglion Cell Biology, Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892.
Stanislav I TomarevSection of Retinal Ganglion Cell Biology, Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892. Electronic address: tomarevs@nei.nih.gov.
National Institutes of Health · USNational Eye Institute · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007309 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI COX, ANDREA L · 1985 to 2019
$43.2M
Molecular Mechanisms Of GlaucomaZIAEY000318 · NEI · NATIONAL EYE INSTITUTE · PI TOMAREV, STANISLAV I · 2009 to 2025
$18.9M
Intramural NIH HHS
6 · The paper itself

Abstract

Myocilin is a secreted glycoprotein that is expressed in ocular and non-ocular tissues. Mutations in the MYOCILIN gene may lead to juvenile- and adult-onset primary open-angle glaucoma. Here we report that myocilin is expressed in bone marrow-derived mesenchymal stem cells (MSCs) and plays a role in their differentiation into osteoblasts in vitro and in osteogenesis in vivo. Expression of myocilin was detected in MSCs derived from mouse, rat, and human bone marrow, with human MSCs exhibiting the highest level of myocilin expression. Expression of myocilin rose during the course of human MSC differentiation into osteoblasts but not into adipocytes, and treatment with exogenous myocilin further enhanced osteogenesis. MSCs derived from Myoc-null mice had a reduced ability to differentiate into the osteoblastic lineage, which was partially rescued by exogenous extracellular myocilin treatment. Myocilin also stimulated osteogenic differentiation of wild-type MSCs, which was associated with activation of the p38, Erk1/2, and JNK MAP kinase signaling pathways as well as up-regulated expression of the osteogenic transcription factors Runx2 and Dlx5. Finally, cortical bone thickness and trabecular volume, as well as the expression level of osteopontin, a known factor of bone remodeling and osteoblast differentiation, were reduced dramatically in the femurs of Myoc-null mice compared with wild-type mice. These data suggest that myocilin should be considered as a target for improving the bone regenerative potential of MSCs and may identify a new role for myocilin in bone formation and/or maintenance in vivo.

Indexed as

AnimalsCell DifferentiationCells, CulturedCore Binding Factor Alpha 1 SubunitCytoskeletal ProteinsExtracellular Signal-Regulated MAP KinasesEye ProteinsGlycoproteinsHomeodomain ProteinsHumansMAP Kinase Signaling SystemMesenchymal Stem CellsMiceMice, Mutant StrainsMyocilinOsteoblastsCore Binding Factor Alpha 1 SubunitCytoskeletal ProteinsDistal-less homeobox proteinsDLX5 protein, humanDlx5 protein, mouseExtracellular Signal-Regulated MAP KinasesEye ProteinsGlycoproteinsHomeodomain ProteinsMyocilinRUNX2 protein, humanRunx2 protein, mouseRunx2 protein, ratTranscription FactorsDifferentiationGlycoprotein SecretionMAP Kinases (MAPKs)Mesenchymal Stem CellsMyocilinOsteogenesisSignaling

Identifiers

PMID23629661
PMCPMC3675621
OpenAlexW2024375815

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.