| Title | G-CSF promotes the viability and angiogenesis of injured liver via direct effects on the liver cells |
| Authors | Liu, Zifeng Zhang, Guiling Chen, Jing Tong, Jingjing Wang, Hongmin Yang, Dong Hu, Jinhua |
| Affiliation | Med Sch Chinese PLA, Beijing, Peoples R China Peoples Liberat Army Gen Hosp, Med Ctr 5, Senior Dept Hepatol, Beijing, Peoples R China Chengwu Peoples Hosp, Dept Pathol, Heze, Peoples R China Beijing Jishuitan, Dept Infect Dis, Beijing, Peoples R China Peking Univ, Clin Med Sch 302, Beijing, Peoples R China Jining Med Univ, Affiliated Hosp, Oncol Dept, Jining, Peoples R China |
| Keywords | ENDOTHELIAL GROWTH-FACTOR IMPROVES SURVIVAL PROLIFERATION REPAIR |
| Issue Date | Jul-2022 |
| Publisher | MOLECULAR BIOLOGY REPORTS |
| Abstract | Background Presently, liver transplantation is the only treatment strategy for liver failure (LF). Although granulocyte-colony stimulating factor (G-CSF) exhibits protective functions in LF, it is not clear whether it directly affects the liver cells. Methods and Results We established an injured liver cell model and observed that G-CSF treatment promoted cell viability and enhanced Ki67 and VEGF-A expression. Thereafter, human umbilical vein endothelial cells (HUVECs) were cultured in a conditioned medium collected from the G-CSF-treated injured liver cells. HUVECs' proliferation and tubule formation were promoted. Furthermore, in an injured liver mouse model, confirmed via haematoxylin-eosin staining, we evaluated serum alanine aminotransferase activity, Ki67 expression, and microvessel density (MVD). G-CSF treatment significantly relieved liver injury, upregulated Ki67 expression, and enhanced MVD in the injured mouse liver tissue. Additionally, AKT and ERK signal targets were explored, and it was demonstrated that the effects of G-CSF on injured liver cells were mediated through the AKT and ERK signalling pathways. Conclusions G-CSF promotes injured liver viability and angiogenesis by directly affecting injured liver cells via the AKT and ERK signalling pathways. These findings improve our understanding of the role of G-CSF in recovery from LF. |
| URI | http://hdl.handle.net/20.500.11897/648744 |
| ISSN | 0301-4851 |
| DOI | 10.1007/s11033-022-07715-4 |
| Indexed | SCI(E) |
| Appears in Collections: | 待认领 |
