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http://repository.pnuh.or.kr/handle/2015.OAK/179
2024-03-28T05:51:28ZMicroRNA-302 induces proliferation and inhibits oxidant-induced cell death in human adipose tissue-derived mesenchymal stem cells
http://repository.pnuh.or.kr/handle/2015.OAK/410
Title(Korean): MicroRNA-302 induces proliferation and inhibits oxidant-induced cell death in human adipose tissue-derived mesenchymal stem cells
Author: 배용찬
Abstract: Mesenchymal stem cells (MSCs) are a heterogeneous population of cells that proliferate in vitro as plastic-adherent cells, have a fibroblast-like morphology, form colonies in vitro and can differentiate into bone, cartilage and fat cells. The abundance, ease and repeatable access to subcutaneous adipose tissue and the simple isolation procedures provide clear advantages for the use of human adipose tissue-derived mesenchymal stem cells (hASDCs) in clinical applications. We screened microRNAs (miRNAs) that affected the proliferation and survival of hADSCs. Transfection of miR-302d mimic increased cell proliferation and protected cells from oxidant-induced cell death in hADSCs, which was supported by flow-cytometric analysis. miR-302d did not affect the expression of Bcl-2 family members or anti-oxidant molecules. The Nrf2-Keap1 system, which is one of the major mechanisms for the cellular defense against oxidative stress, was not altered by transfection of miR-302d mimic. To identify the target of the miR-302d actions on proliferation and survival of hADSCs, a microarray analysis was performed using miR-302d-overexpressing hADSCs. Real-time PCR analysis showed that transfection of miR-302d mimic inhibited the CDKN1A and CCL5 expression. Downregulation of CDKN1A with a specific siRNA mimicked the effect of miR-302d on hADSCs proliferation, but did not affect miR-302d-induced cell survival. Downregulation of CCL5 protected oxidant-induced cell death as miR-302d, inhibited oxidant-induced reactive oxygen species (ROS) generation and the addition of recombinant CCL5 inhibited the protective action of miR-302d on oxidant-induced cell death. This study indicates that miR-302 controls proliferation and cell survival of hADSCs through different targets and that this miRNA can be used to enhance the therapeutic efficacy of hADSCs transplantation in vivo2015-01-01T00:00:00ZBMP2 Increases Adipogenic Differentiation in the Presence of Dexamethasone, which is Inhibited by the Treatment of TNF-alpha in Human Adipose Tissue-Derived Stromal Cells
http://repository.pnuh.or.kr/handle/2015.OAK/399
Title(Korean): BMP2 Increases Adipogenic Differentiation in the Presence of Dexamethasone, which is Inhibited by the Treatment of TNF-alpha in Human Adipose Tissue-Derived Stromal Cells
Author: 배용찬
Abstract: BACKGROUND/AIMS:
The aim of this study was to analyze the effect of BMP2 on osteogenic differentiation of human adipose tissue-derived stromal cells (hADSCs).
METHODS:
Cultured cells were differentiated into osteogenic lineage in the presence of BMP2. Gene expressions were determined by real time PCR.
RESULTS:
BMP2 increased (2/8) or inhibited (6/8) osteogenic differentiation according to hADSCs batches. Regardless of the BMP2 action on osteogenic differentiation, BMP2 induced lipid droplet formation under an osteogenic differentiation condition in all batches of hADSCs, not hBMSCs, to be tested, which was confirmed by analysis of adipogenesis related genes expression. hADSCs expressed various BMP receptors. BMP2 increased expression of BMP2-responsive genes such as DLX3 and ID2, and induced SMAD1 phosphorylation in hADSCs and hBMSCs. BMP2 increased osteogenic differentiation of hADSCs in osteogenic medium in which dexamethasone was omitted. The addition of BMP2 in the control culture media containing dexamethasone alone lead to formation of lipid droplets and increased C/EBP-α expression in hADSCs. In the presence of TNF-α, BMP2 stimulated osteogenic differentiation of hADSCs even in hADSCs batches in which treatment of BMP2 alone inhibited osteogenic differentiation.
CONCLUSION:
These data indicate that the control of osteogenesis and adipogenesis in hADSCs is closely related, and that hADSCs have preferential commitment to adipogenic lineages.2014-01-01T00:00:00Z