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1
High Dose of FGF-2 Induced Growth Retardation via ERK1/2 De-phosphorylation in Bone Marrow-derived Mesenchymal Stem Cells

Kwang Yong Shim,Fatema Tuj Saima,Young Woo Eom 대한의생명과학회 2017 Biomedical Science Letters Vol.23 No.2
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  ScienceON
  
  DBpia
Fibroblast growth factor (FGF)-2 is one of the most effective growth factors to increase the growth rate of mesenchymal stem cells (MSCs). Previously, we reported that low dose of FGF-2 (1 ng/ml) induced proliferation of bone marrowderived mesenchymal stem cells (BMSCs) through AKT and ERK activation resulting in reduction of autophagy and senescence, but not at a high dose. In this study, we investigated the effects of high dose FGF-2 (10 ng/ml) on proliferation, autophagy and senescence of BMSCs for long term cultures (i.e., 2 months). FGF-2 increased the growth rate of BMSCs in a dose dependent manner for a short term (3 days), while during long term cultures (2 months), population doubling time was increased and accumulated cell number was lower than control in BMSCs when cultured with 10 ng/ml of FGF-2. 10 ng/ml of FGF-2 induced immediate de-phosphorylation of ERK1/2, expression of LC3-II, and increase of senescence associated β-galactosidase (SA-β-Gal, senescence marker) expression. In conclusion, we showed that 10 ng/ml of FGF-2 was inadequate for ex vivo expansion of BMSCs because 10 ng/ml of FGF-2 induced growth retardation via ERK1/2 de-phosphorylation and induction of autophagy and senescence in BMSCs.
2
Adipose-derived stem cells ameliorate colitis by suppression of inflammasome formation and regulation of M1-macrophage population through prostaglandin E2

Park, Hong Jun,Kim, Jiye,Saima, Fatema Tuj,Rhee, Ki-Jong,Hwang, Soonjae,Kim, Moon Young,Baik, Soon Koo,Eom, Young Woo,Kim, Hyun-Soo Elsevier 2018 Biochemical and biophysical research communication Vol.498 No.4
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Abstract Inflammatory bowel disease (IBD) is an idiopathic disease caused by a dysregulated immune response to intestinal microbes in an individual with a genetic predisposition. Therefore, alleviation of inflammation is very important to treat IBD. Mesenchymal stem cells (MSCs) have been highlighted as new candidates for treating autoimmune disease based on their immunomodulatory properties. In this study, we investigated the anti-inflammatory mechanism and therapeutic effects of adipose tissue-derived MSCs (ASCs) using THP-1 macrophages and dextran sodium sulfate (DSS)-induced mice with chronic colitis. LPS-treated THP-1 cells expressed mRNA of CD11b, an M1 macrophage marker, at day 2. However, THP-1 co-cultured with ASCs expressed mRNA of CD206, CD68, CCL18, legumain, and IL-10, markers of M2 macrophages. In THP-1 cells co-cultured with ASCs, precursor (pro)-IL-1β, Cox-2, and NLRP3 increased dramatically compared to LPS-treated THP-1 cells. Secretion of IL-1β and IL-18 was significantly inhibited by ASCs, but PGE2 production was highly increased in co-culture conditions of THP-1 and ASCs. IL-18 secretion was inhibited by PGE2 treatment, and PGE2 inhibited inflammasome complex (ASC/Cas-1/NLRP3) formation in THP-1 cells. In the DSS-induced chronic colitis model, ASCs ameliorated colitis by decreasing the total number of macrophages and the M1 macrophage population. Our results suggest that ASCs can suppress the inflammatory response by controlling the macrophage population, and ASCs may be therapeutically useful for the treatment of IBD. Highlights <UL> <LI> PGE2 was remarkably increased in conditioned media from THP-1 co-cultured with ASCs. </LI> <LI> ASCs induced M1 to M2 macrophage transition through PGE2. </LI> <LI> ASCs suppressed secretion of inflammatory IL-1β and IL-18 through PGE2. </LI> <LI> ASCs ameliorated colitis by decreasing the total number of macrophages. </LI> <LI> ASCs relieved inflammation by decreasing the M1 macrophage population. </LI> </UL>