Protective effects of hepatocyte growth factor on hypoxic human pulmonary microvascular endothelial cells.
- Author:
Na GUO
1
;
Ying-hua GUO
;
Long-xiang SU
;
Ya-juan WANG
;
Yan LIU
;
Xue-ge JIANG
;
Chang-ting LIU
Author Information
- Publication Type:Journal Article
- MeSH: Cell Adhesion; drug effects; Cell Hypoxia; Cell Survival; drug effects; Cells, Cultured; Endothelial Cells; drug effects; Endothelium, Vascular; cytology; metabolism; Hepatocyte Growth Factor; pharmacology; Humans; Intercellular Adhesion Molecule-1; metabolism; Lung; blood supply
- From: Acta Academiae Medicinae Sinicae 2013;35(1):1-5
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the protective effects of hepatocyte growth factor (HGF) on hypoxic human pulmonary microvascular endothelial cells (HPMECs).
METHODSHPMECs were cultured in vitro, and the hypoxic model was established by the physical method. Cells were divided into 4 groups: the control group, the hypoxic group, HGF group, and phytohemagglutinin (PHA) group. The 7(th) generation of HPMECs was evaluated by the method of immunocytochemistry. The persistence rate of HPMECs was measured by MTT assay and the adhesive cells were counted by the microscopy. The expression of intercellular adhesion molecule-1 (ICAM-1) protein was determined by immunofluorescence staining.
RESULTSThe adherence percentage of cells significantly decreased after hypoxia, whereas the expression of the ICAM-1 protein was significantly higher in the hypoxia group than in control group (P<0.01). Compared with the hypoxia group, the persistence and adherence percentage of cells in the HGF group significantly increased (P<0.01), whereas the expression of the ICAM-1 protein significantly dropped (P<0.01). In the PHA group, the persistence and adhesion rate were significantly different from those in the hypoxia group and HGF group (P<0.01), and the expression of the ICAM-1 protein increased significantly (P<0.01).
CONCLUSIONHGF could inhibit the hypoxic damage of HPMECs by decreasing the persistence and the adhesive capacity of these cells and inducing the expression of ICAM-1.
