Detailed Abstract
[E-poster]
[EP054] A novel antifibrotic strategy utilizing conditioned media obtained from miR-150-transfected adipose-derived stem cells: validation in an animal model of liver fibrosis
Kwang Yeol PAIK1, Tae Ho HONG5, Ho Joong CHOI5, Jung Hyun PARK2, Kee-Hwan KIM3, Dong Do YOU4, Jae Hyun HAN4, Say-June KIM*5
1Department of Surgery, Yeouido ST. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Korea
2Department of Surgery, Eunpeong St. Mary's Hospital, College of Medicine, the Catholic University of Korea, Korea
3Department of Surgery, Uijeongbu St. Mary's Hospital, College of Medicine, the Catholic University of Korea, Korea
4Department of Surgery, St. Paul's Hospital, College of Medicine, the Catholic University of Korea, Korea
5Department of Surgery, Seoul St. Mary’s Hospital, College of Medicine, the Catholic University of Korea, Korea
Introduction : The limitations of stem cells have led researchers to investigate the secretome, the total collection of secretory materials from stem cells, since the principal mechanism of action of stem cells is mediated by the secretome. In this study, we determined the antifibrotic potential of the secretome released from miR-150-transfected adipose-derived stromal cells (ASCs).
Methods : To validate antifibrotic effects of the miR-150-secretome, we generated in vitro and in vivo models of liver fibrosis by the treatment of human hepatic stellate cells (LX2 cells) with thioacetamide (TAA) and the subcutaneous injection of TAA into mice, respectively. In an in vitro model, more significant reductions in the expression of fibrosis-related markers, such as TGFβ, Col1A1, and α-SMA, were observed using the miR-150-secretome than the control secretome, especially in TAA-treated LX2 cells. In an in vivo experiment, the infusion of the miR-150-secretome into mice with liver fibrosis induced 1) a reduction in the elevation of serum levels of systemic inflammatory cytokines, such as IL-6 and TNF-α, and 2) higher expression of markers of anti-fibrosis, proliferation, and antioxidant activity in the liver.
Results : Our in vitro and in vivo experiments indicate that the miR-150-secretome is superior to the naïve secretome in terms of ameliorating liver fibrosis, minimizing systemic inflammatory responses, and promoting antioxidant enzyme expression.
Conclusions : We conclude that miR-150 transfection into ASCs has the potential to induce the release of secretory materials with enhanced antifibrotic, proliferative, and antioxidant properties.
Methods : To validate antifibrotic effects of the miR-150-secretome, we generated in vitro and in vivo models of liver fibrosis by the treatment of human hepatic stellate cells (LX2 cells) with thioacetamide (TAA) and the subcutaneous injection of TAA into mice, respectively. In an in vitro model, more significant reductions in the expression of fibrosis-related markers, such as TGFβ, Col1A1, and α-SMA, were observed using the miR-150-secretome than the control secretome, especially in TAA-treated LX2 cells. In an in vivo experiment, the infusion of the miR-150-secretome into mice with liver fibrosis induced 1) a reduction in the elevation of serum levels of systemic inflammatory cytokines, such as IL-6 and TNF-α, and 2) higher expression of markers of anti-fibrosis, proliferation, and antioxidant activity in the liver.
Results : Our in vitro and in vivo experiments indicate that the miR-150-secretome is superior to the naïve secretome in terms of ameliorating liver fibrosis, minimizing systemic inflammatory responses, and promoting antioxidant enzyme expression.
Conclusions : We conclude that miR-150 transfection into ASCs has the potential to induce the release of secretory materials with enhanced antifibrotic, proliferative, and antioxidant properties.
SESSION
E-poster
E-Session 7/27 ~ 7/29 ALL DAY