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Updated: Jan 2, 2026

An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function
Published on: May 4, 2021
MicroRNA-150 Modulates Adipogenic Differentiation of Adipose-Derived Stem Cells by Targeting Notch3
Xiang Li1, Yu Zhao2,3, Xiuquan Li2
1Department of Cell Biology, Key Laboratory of Cell Biology, Ministry of Public Health, and Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, Liaoning 110122, China.
Abstract:
MicroRNAs (miRNAs) influence stem cell functions, including mobilization, proliferation, and differentiation. miR-150 is abundantly expressed in monocytes. Knockdown of miR-150 promotes bone marrow stem cell migration. The role of miR-150 in adipose-derived stem cells (ADSCs) is unclear. In this study, the effects of miR-150 on adipogenic differentiation and proliferation of ADSCs were investigated. ADSCs were isolated from the inguinal adipose tissue of wild-type (WT) and miR-150 knockout (KO) mice and were induced for adipogenic differentiation. The miR-150 level was detected by real-time PCR. ADSCs were transfected by miR-150 or small-interfering RNA (siRNA) of Notch3. MTT assay and colony formation assay were performed in miR-150 knockdown and control ADSCs. Real-time PCR showed that miR-150 was expressed in ADSCs. miR-150 knockdown significantly decreased the capacity of adipogenic differentiation of ADSCs, as compared with their counterparts from WT mice. It is intriguing that the overexpression of miR-150 significantly increased C/EBPα and PPAR-γ expression and lipid formation in ADSCs with adipogenic induction. Overexpression of miR-150 significantly decreased Notch3 expression in ADSCs compared with the control groups. Furthermore, Notch3 inhibition promoted the adipogenic differentiation in ADSCs. miR-150 also suppressed proliferation potential and the expression of Nanog in ADSCs. In summary, this study demonstrates, for the first time, that miR-150 promotes adipogenic differentiation and inhibits proliferation of ADSCs. miR-150 regulates adipogenic differentiation of ADSCs, likely mediated by the downregulation of Notch3.
Insights
MicroRNA-150 (miR-150) promotes the differentiation of adipose-derived stem cells (ADSCs) into fat cells while inhibiting their proliferation. This regulation is likely mediated by downregulating Notch3 signaling in ADSCs.
Area of Science:
- Stem Cell Biology
- Molecular Biology
- Epigenetics
Background:
- MicroRNAs (miRNAs) are key regulators of stem cell functions, including differentiation and proliferation.
- miR-150 is known to affect monocyte function and bone marrow stem cell migration.
- The specific role of miR-150 in adipose-derived stem cells (ADSCs) remained largely uncharacterized.
Purpose of the Study:
- To investigate the role of miR-150 in the adipogenic differentiation of ADSCs.
- To examine the effect of miR-150 on ADSC proliferation.
- To elucidate the molecular mechanism, particularly the involvement of Notch3, in miR-150's function within ADSCs.
Main Methods:
- Isolation and culture of ADSCs from wild-type (WT) and miR-150 knockout (KO) mice.
- Induction of adipogenic differentiation and assessment of differentiation markers (C/EBPα, PPAR-γ, lipid formation).
- Transfection of ADSCs with miR-150 mimics or Notch3 siRNA, followed by proliferation assays (MTT, colony formation) and gene expression analysis (real-time PCR).
Main Results:
- miR-150 was expressed in ADSCs, and its knockdown significantly impaired adipogenic differentiation.
- Overexpression of miR-150 enhanced adipogenic differentiation, increasing key adipogenic markers and lipid accumulation.
- miR-150 overexpression suppressed ADSC proliferation and Nanog expression, while it downregulated Notch3 expression; Notch3 inhibition promoted adipogenesis.
Conclusions:
- miR-150 plays a crucial role in promoting adipogenic differentiation of ADSCs.
- miR-150 inhibits the proliferation potential of ADSCs.
- The pro-adipogenic effect of miR-150 on ADSCs is likely mediated through the downregulation of Notch3.
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