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

Background.Since thefirst 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 lymphocytereaction (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 factorβ1 (TGF-β1) in ADSC-CM. The transcriptabundance of TGF-β1, as well as that of insulin-like growth factor binding protein 3 (IGF-BP3), was evaluated using qRT-PCRon 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 ofJurkat cell proliferation.Results.Thefindings confirm that the isolated ADSCs demonstrate classic ADSC characteristics. Thelevel of TGF-β1 was found to be low in ADSC-CM, as assessed by ELISA. Jurkat cells grown in ADSC-CM show reduced geneexpression of TGF-β1 and IGF-BP3 compared with that of the control group. Furthermore, western blotting of ADSC-CMgrown Jurkat cells that were blocked at the G0/G1 stage indicates that ADSC-CM decreases the protein expression of pP38 in adose-dependent manner.Conclusion.ADSC-CM can inhibit Jurkat cell proliferation through the TGF-β1-p38 signaling pathway.