2. Academic Validation
  3. G-CSF promotes the viability and angiogenesis of injured liver via direct effects on the liver cells

G-CSF promotes the viability and angiogenesis of injured liver via direct effects on the liver cells

  • Mol Biol Rep. 2022 Sep;49(9):8715-8725. doi: 10.1007/s11033-022-07715-4.
Zifeng Liu 1 2,  Guiling Zhang 3,  Jing Chen 1 2,  Jingjing Tong 1 4,  Hongmin Wang 2 5,  Jing Chen 1,  Dong Yang 6,  Jinhua Hu 7 8 9
Affiliations

Affiliations

  • 1 Medical School of Chinese PLA, Beijing, China.
  • 2 Senior Department of Hepatology, The Fifth Medical Center of PLA General Hospital, Beijing, China.
  • 3 Department of Pathology, Chengwu People's Hospital, Heze, China.
  • 4 Department of Infectious Diseases, Beijing Jishuitan, Beijing, China.
  • 5 Peking University 302 Clinical Medical School, Beijing, China.
  • 6 Oncology Department, Affiliated Hospital of Jining Medical University, Jining, China.
  • 7 Medical School of Chinese PLA, Beijing, China. 13910020608@163.com.
  • 8 Senior Department of Hepatology, The Fifth Medical Center of PLA General Hospital, Beijing, China. 13910020608@163.com.
  • 9 Peking University 302 Clinical Medical School, Beijing, China. 13910020608@163.com.
PMID: 35781603 DOI: 10.1007/s11033-022-07715-4
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.

Keywords

Angiogenesis; Cell viability; Granulocyte-colony stimulating factor; Liver failure; Vessel endothelial growth factor A.

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