Emodin suppresses adipogenesis of bone marrow derived mesenchymal stem cells from aplastic anemia via increasing TRIB3 expression.

Autor: Zhang X; Medical Research Center, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China., Liu L; Medical Research Center, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China., Wang J; Department of Hematology, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China., Yao M; Department of Hematology, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China., Liu L; Department of Hematology, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China., Liu H; Department of Hematology, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China., Ren S; Department of Hematology, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China., Wei P; Department of Radiation Oncology, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China., Cheng P; Department of Hematology, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China., Li X; Department of Graduate School, Jining Medical University, Jining 272000, Shandong Province, China., Zhang H; Department of Hematology, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China. Electronic address: gx-zhanghao@126.com., Chen M; Medical Research Center, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China. Electronic address: chenmt3153@mail.jnmc.edu.cn.
Jazyk: angličtina
Zdroj: Tissue & cell [Tissue Cell] 2024 Feb; Vol. 86, pp. 102287. Date of Electronic Publication: 2023 Dec 10.
DOI: 10.1016/j.tice.2023.102287
Abstrakt: Background: Increasing evidence indicate that enhanced adipogenic differentiation of bone marrow mesenchymal stem cells (BM-MSCs) could contribute to the adiposity alteration in marrow microenvironment of aplastic anemia (AA). Identifying small molecule drugs with role in inhibiting adipogenesis of BM-MSCs may represent a novel direction in AA therapy by improving BM-MSCs mediated marrow microenvironment.
Methods: For the purpose, we isolated AA BM-MSCs through whole bone marrow cell culture, evaluated a series of small molecule drugs using the in vitro adipogenic differentiation model of BM-MSCs, and finally focused on emodin, a natural anthraquinone derivative. Subsequently, we systematically investigated the molecular mechanism of emodin in attenuating adipogenic process by means of microarray profiling, bioinformatics analysis and lentivirus-mediated functional studies and rescue assay.
Results: We found that emodin presented significantly suppressive effect on the in vitro adipogenic differentiation of AA BM-MSCs. Further mechanistic investigation revealed that emodin could increase the expression of Tribbles homolog 3 (TRIB3) which exhibited remarkably decreased expression in AA BM-MSCs compared with the normal counterparts and was subsequently demonstrated as a negative regulator in adipogenesis of AA BM-MSCs. Besides, TRIB3 depletion alleviated the suppressive effect of emodin on the adipogenic differentiation of AA BM-MSCs.
Conclusion: Our findings propose that emodin mediated TRIB3 up-regulation alleviates the adipogenic capacity of AA BM-MSCs, and emodin could serve as a potential therapeutic regimen for AA therapy.
Competing Interests: Declaration of Competing Interest The authors declare no competing interests.
(Copyright © 2023 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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