The effect of electromagnetic fields on the proliferation and the osteogenic or adipogenic differentiation of mesenchymal stem cells modulated by dexamethasone.

Bioelectromagnetics · 2014 · Benefit · Low evidence

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BenefitLow evidencePaper 4668

Study snapshot

PublicationBioelectromagnetics · 2014

Study typein_vitro

Reported directionBenefit

Evidence ratingLow

Abstract

Although glucocorticoids provide benefits for inflammation or autoimmune disorders, high-dose and long-term use could cause osteonecrosis or osteoporosis as adverse effect for patients. Electromagnetic field (EMF) treatments have been clinically used for many years to promote fracture healing, but whether EMF can attenuate the deleterious effects of glucocorticoids is not clear. In this study, the effects of different concentrations of dexamethasone (DEX) on proliferation and adipogenic or osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) were detected and compared, and the effects of EMF treatment (15 Hz, 1 mT, 4 h/day) on 0.1 µM DEX-modulated BMSCs' proliferation and adipogenic or osteogenic differentiation were investigated. Higher concentrations of DEX (0.1 and 1 µM) inhibited proliferation of BMSCs but promoted expression of adipogenic-related genes, increasing the number of lipid droplets. In the early stage of differentiation, DEX restrained expression of RUNX2 and alkaline phosphatase (ALP), but amplified expression of ALP and osteopontin (OPN) in the late stage. EMF treatment of BMSCs influenced by 0.1 µM DEX inhibited the high expression of adipogenic-related genes, stimulated the expression of RUNX2, ALP, OPN, and osteocalcin, and increased the activity of ALP. EMF exposure augmented the expression of p-ERK, which DEX reduced. After using mitogen-activated protein/extracellular signal-regulated kinase (ERK) kinase (MEK)/ERK signaling pathway inhibitor, U0126, the effect of EMF was reduced. In conclusion, EMF exposure accelerates BMSCs proliferation, inhibits adipogenic differentiation, and promotes osteogenic differentiation of BMSCs modulated by DEX, and these effects are mediated at least in part by MEK/ERK signaling pathway.

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AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typein_vitro

Effect directionbenefit

PopulationBone marrow mesenchymal stem cells (BMSCs)

Sample sizeNot supplied

ExposureELF · 4 h/day

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

Higher dexamethasone concentrations (0.1 and 1 µM) inhibited BMSC proliferation and increased adipogenic-related gene expression and lipid droplets. EMF treatment (15 Hz, 1 mT, 4 h/day) in 0.1 µM DEX-modulated BMSCs inhibited adipogenic-related gene expression and increased osteogenic markers (RUNX2, ALP, OPN, osteocalcin) and ALP activity; EMF also increased p-ERK expression, and the EMF effect was reduced by the MEK/ERK inhibitor U0126.

Outcomes measured

BMSC proliferation
Adipogenic differentiation (adipogenic-related gene expression, lipid droplets)
Osteogenic differentiation (RUNX2, ALP, OPN, osteocalcin; ALP activity)
p-ERK expression
Effect modification by MEK/ERK inhibitor (U0126)

Limitations

In vitro study (cell culture), limiting direct inference to clinical outcomes
Sample size not reported in provided abstract
Only one EMF condition (15 Hz, 1 mT, 4 h/day) and one DEX concentration (0.1 µM) tested for EMF effects in the abstract

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": "ELF",
    "source": "other",
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": "4 h/day"
  },
  "population": "Bone marrow mesenchymal stem cells (BMSCs)",
  "sample_size": null,
  "outcomes": [
    "BMSC proliferation",
    "Adipogenic differentiation (adipogenic-related gene expression, lipid droplets)",
    "Osteogenic differentiation (RUNX2, ALP, OPN, osteocalcin; ALP activity)",
    "p-ERK expression",
    "Effect modification by MEK/ERK inhibitor (U0126)"
  ],
  "main_findings": "Higher dexamethasone concentrations (0.1 and 1 µM) inhibited BMSC proliferation and increased adipogenic-related gene expression and lipid droplets. EMF treatment (15 Hz, 1 mT, 4 h/day) in 0.1 µM DEX-modulated BMSCs inhibited adipogenic-related gene expression and increased osteogenic markers (RUNX2, ALP, OPN, osteocalcin) and ALP activity; EMF also increased p-ERK expression, and the EMF effect was reduced by the MEK/ERK inhibitor U0126.",
  "effect_direction": "benefit",
  "limitations": [
    "In vitro study (cell culture), limiting direct inference to clinical outcomes",
    "Sample size not reported in provided abstract",
    "Only one EMF condition (15 Hz, 1 mT, 4 h/day) and one DEX concentration (0.1 µM) tested for EMF effects in the abstract"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "electromagnetic field",
    "ELF-EMF",
    "15 Hz",
    "1 mT",
    "dexamethasone",
    "glucocorticoid",
    "bone marrow mesenchymal stem cells",
    "BMSCs",
    "proliferation",
    "adipogenesis",
    "osteogenesis",
    "RUNX2",
    "ALP",
    "osteopontin",
    "osteocalcin",
    "ERK",
    "MEK/ERK signaling",
    "U0126"
  ],
  "suggested_hubs": []
}

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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.1002/bem.21867
PubMed: 25145543

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