Level C· Early human research exploring benefitsProspective StudyPubMedOpen access

miR‑30a‑5p induces the adipogenic differentiation of bone marrow mesenchymal stem cells by targeting FAM13A/Wnt/β‑catenin signaling in aplastic anemia.

Wang E., Zhang Y., Ding R., Wang X., Zhang S., Li X.

Prospective Study, published in Mol Med Rep (2021) — summary generated from the PubMed abstract.

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Level C· Early human research exploring benefitsEvidence level of this study

Early human evidence such as case series or small samples is exploring possible benefits.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Prospective Study
Journal
Mol Med Rep (2021)
Country
Greece
Reported sample size
—
Source database
PubMed
PMID
34821370
PMCID
PMC8630822
DOI
10.3892/mmr.2021.12543
Citations
9

Abstract (original English)

Aplastic anemia (AA) is a bone marrow failure syndrome with high morbidity and mortality. Bone marrow (BM)‑mesenchymal stem cells (MSCs) are the main components of the BM microenvironment, and dysregulation of BM‑MSC adipogenic differentiation is a pathologic hallmark of AA. MicroRNAs (miRNAs/miRs) are crucial regulators of multiple pathological processes such as AA. However, the role of miR‑30a‑5p in the modulation of BM‑MSC adipogenic differentiation in AA remains unclear. The present study aimed to explore the effect of miR‑30a‑5p on AA BM‑MSC adipogenic differentiation and the underlying mechanism. The levels of miR‑30a‑5p expression and family with sequence similarity 13, member A (FAM13A) mRNA expression in BM‑MSCs were quantified using reverse transcription‑quantitative (RT‑q) PCR. The mRNA expression levels of adipogenesis‑associated factors [fatty acid‑binding protein 4 (FABP4), lipoprotein lipase (LPL), perilipin‑1 (PLIN1), peroxisome proliferator‑activated receptor γ (PPARγ) and CCAAT/enhancer binding protein α (C/EBPα)] were analyzed using RT‑qPCR. Lipid droplet accumulation was evaluated using Oil Red O staining in BM‑MSCs. The interaction between miR‑30a‑5p and the FAM13A 3'‑untranslated region was identified by TargetScan, and a dual‑luciferase reporter assay was used to confirm the interaction. The expression levels of FAM13A and Wnt/β‑catenin pathway‑related pr

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

How we grade evidence
AdipogenesisAdipose TissueAdultAnemia, AplasticBone Marrow CellsCCAAT-Enhancer-Binding Protein-alphaCell DifferentiationFatty Acid-Binding ProteinsFemaleGTPase-Activating Proteins

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