Downregulation of microRNA‑143 promotes osteogenic differentiation of human adipose‑derived mesenchymal stem cells through the k‑Ras/MEK/ERK signaling pathway.
Zhang Y., Zhou K., Wu L., Gu H., Huang Z., Xu J.
Laboratory Study, published in Int J Mol Med (2020) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- 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
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
- Laboratory Study
- Journal
- Int J Mol Med (2020)
- Country
- Greece
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 32582994
- PMCID
- PMC7388841
- DOI
- 10.3892/ijmm.2020.4651
- Citations
- 11
Abstract (original English)
MicroRNAs (miRNAs) are known to have regulatory roles in the osteogenic differentiation of various mesenchymal stem cells (MSCs), although their regulatory role on human adipose‑derived mesenchymal stem cells (hADSCs) remains unclear. The aim of the present study was to investigate the biological function and underlying molecular mechanism of miRNAs in regulating the osteogenic differentiation of hADSCs using microarray assay. hADSCs differentiated into osteoblasts under culture with osteogenic medium, with an increase observed in calcium deposits and alkaline phosphatase activity. The mRNA levels of bone sialoprotein, osteopontin and osteocalcin increased, whereas Runt‑related transcription factor‑2 expression decreased during osteogenic differentiation. In addition, miR‑143 was markedly downregulated during osteogenic differentiation, while miR‑143 overexpression inhibited and miR‑143 knockdown enhanced this process. miR‑143 overexpression also blocked extracellular signal‑regulated kinase 1/2 (ERK1/2) pathway activation, while miR‑143 inhibition enhanced it. The promoting effects of miR‑143 knockdown on the osteogenic differentiation of hADSCs were partly diminished by the mitogen‑activated protein kinase (MEK) inhibitors U0126 and PD98059. Bioinformatics analysis further revealed that miR‑143 targets k‑Ras and directly binds to the 3'‑untranslated region of its mRNA. Inhibi
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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