Conditioned Medium from Adipose-Derived Stem Cell Inhibits Jurkat Cell Proliferation through TGF-β1 and p38/MAPK Pathway

• Published in: Analytical cellular pathology (Amsterdam) Vol. 2019; no. 2019; pp. 1 - 6
• Main Authors: Liu, Fei, Zhou, Xianyu, Wang, Yinmin, Wang, Xiuxia
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01.01.2019; Hindawi; Wiley
• ISSN: 2210-7177; 2210-7185
• DOI: 10.1155/2019/2107414

Background. Since the first report on the immunomodulatory and immunosuppressive properties of Adipose-Derived Stem Cells (ADSCs), many studies have elucidated the underlying molecular mechanism of their suppressive activity on mixed lymphocyte reaction (MLR). However, a gap exists in our understanding of the molecular mechanism of ADSC-conditioned medium (ADSC-CM) on MLR. Methods. ADSCs were isolated from Human Adipose Tissues, and Enzyme-linked Immunosorbent Assay (ELISA) was used to identify the concentration of transforming growth factor β1 (TGF-β1) in ADSC-CM. The transcript abundance of TGF-β1, as well as that of insulin-like growth factor binding protein 3 (IGF-BP3), was evaluated using qRT-PCR on Jurkat cells cultured in ADSC-CM for 24 hours. The proliferation of the Jurkat cells was assessed using cell cycle assay. Western blotting was performed to identify potential signaling molecules involved in the ADSC-CM-induced inhibition of Jurkat cell proliferation. Results. The findings confirm that the isolated ADSCs demonstrate classic ADSC characteristics. The level of TGF-β1 was found to be low in ADSC-CM, as assessed by ELISA. Jurkat cells grown in ADSC-CM show reduced gene expression of TGF-β1 and IGF-BP3 compared with that of the control group. Furthermore, western blotting of ADSC-CM grown Jurkat cells that were blocked at the G0/G1 stage indicates that ADSC-CM decreases the protein expression of pP38 in a dose-dependent manner. Conclusion. ADSC-CM can inhibit Jurkat cell proliferation through the TGF-β1-p38 signaling pathway.