ArticleYonsei medical journal2019
MicroRNA-138 Suppresses Adipogenic Differentiation in Human Adipose Tissue-Derived Mesenchymal Stem Cells by Targeting Lipoprotein Lipase.
Article in Yonsei medical journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- miR-10b-5p regulates adipocyte lineage commitment and adipogenesis via targeting of Gata6 and Tubby.Cell communication and signaling : CCS · 2026Article
- Placental mRNA and miRNA dynamics associated with lipid metabolism pathways in pregnancies affected by obesity.Frontiers in endocrinology · 2025Article
- lpla (lipoprotein lipase a) is a marker of early adipogenesis rather than late adipogenesis in grass carp (Ctenopharyngodon idellus).Fish physiology and biochemistry · 2023Article
- MicroRNA-138: an emerging regulator of skeletal development, homeostasis, and disease.American journal of physiology. Cell physiology · 2023Review
- Article
- Regulation of adipogenesis by exosomal milk miRNA.Reviews in endocrine & metabolic disorders · 2023Review
- Review
- Effect of MicroRNA-138 on Tumor Necrosis Factor-Alpha-Induced Suppression of Osteogenic Differentiation of Dental Pulp Stem Cells and Underlying Mechanism.BioMed research international · 2022Article
- Nuclear Receptors and Lipid Sensing.Advances in experimental medicine and biology · 2022Article
- Adipocyte, Immune Cells, and miRNA Crosstalk: A Novel Regulator of Metabolic Dysfunction and Obesity.Cells · 2021Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
purposeAdipogenic differentiation of adipose tissue-derived mesenchymal stem cells (AMSCs) is critical to many disease-related disorders, such as obesity and diabetes. Studies have demonstrated that miRNA-138 (miR-138) is closely involved in adipogenesis. However, the mechanisms affected by miR-138 remain unclear. This work aimed to investigate interactions between miR-138 and lipoprotein lipase (LPL), a key lipogenic enzyme, in AMSCs. MATERIALS AND
methodsHuman AMSCs (hAMSCs) isolated from human abdomen tissue were subjected to adipogenic differentiation medium. Quantitative real-time polymerase chain reaction and Western blot assay were applied to measure the expressions of miR-138, LPL, and the two adipogenic transcription factors cytidine-cytidine-adenosine-adenosine-thymidine enhancer binding protein alpha (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ). The relationship between miR-138 and LPL was predicted utilizing the miRTarBase database and validated by dual luciferase reporter assay.
resultsShowing increases in C/EBPα and PPARγ expression levels, hAMSCs were induced into adipogenic differentiation. During adipogenesis of hAMSCs, miR-138 expression was significantly downregulated. Overexpression of miR-138 by transfection inhibited hAMSCs adipogenic differentiation in vitro. Mechanically, LPL was a target of miR-138. LPL expression was upregulated during adipogenesis of hAMSCs, and this upregulation was reversed by miR-138 overexpression. Functionally, silencing of LPL by transfection exerted similar inhibition of the expressions of C/EBPα and PPARγ. Meanwhile, LPL ectopic expression was able to partly abolish the suppressive effect of miR-138 overexpression on adipogenic differentiation of hAMSCs.
conclusionUpregulation of miR-138 inhibits adipogenic differentiation of hAMSCs by directly downregulating LPL.
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