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

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

  • Tissue Cell. 2023 Dec 10:86:102287. doi: 10.1016/j.tice.2023.102287.
Xianning Zhang 1,  Lulu Liu 1,  Jian Wang 2,  Mingkang Yao 2,  Lei Liu 2,  Haihui Liu 2,  Saisai Ren 2,  Peng Wei 3,  Panpan Cheng 2,  Xiyu Li 4,  Hao Zhang 5,  Mingtai Chen 6
Affiliations

Affiliations

  • 1 Medical Research Center, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China.
  • 2 Department of Hematology, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China.
  • 3 Department of Radiation Oncology, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China.
  • 4 Department of Graduate School, Jining Medical University, Jining 272000, Shandong Province, China.
  • 5 Department of Hematology, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China. Electronic address: [email protected].
  • 6 Medical Research Center, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong Province, China. Electronic address: [email protected].
PMID: 38086146 DOI: 10.1016/j.tice.2023.102287
Abstract

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.

Keywords

Adipogenesis; Aplastic anemia; Bone marrow mesenchymal stem cells; Emodin; TRIB3.

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