Conditioned Medium from Adipose-Derived Stem Cell Inhibits Jurkat Cell Proliferation through TGF-β1 and p38/MAPK
Xiuxia Wang1, Yinmin Wang1,2, Xianyu Zhou1
1Department of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.
Analytical Cellular Pathology (Amsterdam)
|January 15, 2020
Summary
Adipose-Derived Stem Cell conditioned medium (ADSC-CM) inhibits Jurkat cell proliferation. This effect is mediated by the transforming growth factor beta 1 (TGF-β1) and p38 signaling pathway, revealing a key mechanism in immune modulation.
Area of Science:
- Immunology
- Stem Cell Biology
- Molecular Biology
Background:
- Adipose-Derived Stem Cells (ADSCs) possess immunomodulatory properties.
- The molecular mechanisms of ADSC-conditioned medium (ADSC-CM) on mixed lymphocyte reaction (MLR) remain incompletely understood.
Purpose of the Study:
- To investigate the molecular mechanisms by which ADSC-CM affects Jurkat cell proliferation.
- To elucidate the role of specific signaling pathways in ADSC-CM-mediated immunosuppression.
Main Methods:
- ADSCs were isolated, and ADSC-CM was analyzed for transforming growth factor beta 1 (TGF-β1) concentration using ELISA.
- Jurkat cells were cultured in ADSC-CM, and gene expression of TGF-β1 and insulin-like growth factor binding protein 3 (IGF-BP3) was assessed via qRT-PCR.
- Cell cycle analysis and Western blotting were employed to evaluate Jurkat cell proliferation and signaling pathway activation.
Main Results:
- ADSC-CM exhibited low levels of TGF-β1.
- Jurkat cells in ADSC-CM showed reduced gene expression of TGF-β1 and IGF-BP3.
- ADSC-CM dose-dependently decreased p38 protein expression in Jurkat cells, correlating with G0/G1 cell cycle arrest.
Conclusions:
- ADSC-CM effectively inhibits Jurkat cell proliferation.
- The TGF-β1-p38 signaling pathway is a key mediator of ADSC-CM's inhibitory effects on Jurkat cells.
