4.6 Article

Conditioned medium from human tonsil-derived mesenchymal stem cells inhibits glucocorticoid-induced adipocyte differentiation

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PLOS ONE
卷 17, 期 6, 页码 -

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PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0266857

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资金

  1. National Research Foundation of Korea - Ministry of Science and ICT [2017R1E1A1A01073021, 2020R1C1C1014665]
  2. Ewha Womans University
  3. National Research Foundation of Korea [2017R1E1A1A01073021, 2020R1C1C1014665] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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This study found that conditioned medium obtained from human tonsil-derived MSCs (T-MSC CM) can inhibit adipocyte differentiation by regulating glucocorticoid signal transduction, thereby reducing obesity. The experiments showed that T-MSC CM can attenuate early-stage adipocyte differentiation and protect mice from the negative effects induced by glucocorticoid treatment. Additionally, T-MSC CM enhances megakaryocyte differentiation and protects blood platelet counts.
Obesity, which has become a major global health problem, involves a constitutive increase in adipocyte differentiation signaling. Previous studies show that mesenchymal stem cells (MSCs) induce weight loss and glycemic control. However, the mechanisms by which MSCs regulate adipocyte differentiation are not yet known. In this study, we investigated the effects of conditioned medium obtained from human tonsil-derived MSCs (T-MSC CM) on adipocyte differentiation. We found that T-MSC CM attenuated adipocyte differentiation from early stages via inhibiting glucocorticoid signaling. T-MSC CM also increased the phosphorylation of p38 mitogen-activated protein kinase and glucocorticoid receptors and decreased the subsequent nucleus translocation of glucocorticoid receptors. Chronic treatment of mice with synthetic glucocorticoids induced visceral and bone marrow adipose tissue expansion, but these effects were not observed in mice injected with T-MSC CM. Furthermore, T-MSC CM injection protected against reductions in blood platelet counts induced by chronic glucocorticoid treatment, and enhanced megakaryocyte differentiation was also observed. Collectively, these results demonstrate that T-MSC CM exerts inhibitory effects on adipocyte differentiation by regulating glucocorticoid signal transduction. These findings suggest that the therapeutic application of T-MSC CM could reduce obesity by preventing adipose tissue expansion.

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