LPS increases plasminogen activator inhibitor type-1 expression in human endothelial cells
- VernacularTitle:LPS促进HUVECs表达纤溶酶原激活物抑制物1
- Author:
Xiaolong TANG
;
Zhenyou JIANG
;
Huadong WANG
;
Shuyu CAI
- Publication Type:Journal Article
- Keywords:
Lipopolysaccharides;
Tissue plasminogen activator;
Human umbilical vein endothelial cells
- From:
Chinese Journal of Pathophysiology
1986;0(04):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: The aim of this study is to elucidate the effects of lipopolysaccharide (LPS) on tissue plasminogen activator(tPA) and plasminogen activator inhibitor type-1(PAI-1) expression and secretion in endothelial cells. METHODS: Cultured human umbilical vein endothelial cells (HUVECs) were induced by LPS for different times. Cell viability was then determined by cell counting kit-8. tPA and PAI-1 activities in the media were assayed by fibrin overlay and reverse fibrin autograph, respectively. Cytoplasmic RNA was prepared using the Trizol method and was assayed for PAI-I and tPA mRNA levels by reverse transcript-polymerase chain reaction(RT-PCR). RESULTS: LPS(10 mg/L) did not produce cell toxicity according to LDH determination in culture media. PAI-1 activity in LPS group was high (P0.05). CONCLUSION: LPS (10 mg/L) did not show signs of cell toxicity, but promoted the expression of PAI-1 mRNA and induced an increase activity of PAI-1. However, LPS (10 mg/L) did not change tPA mRNA expression. The time-dependent increase in PAI-1 mRNA expression and activity shifts the local balance toword increased anti-fibrinolytic capacity, which can amplify the extent of acute thrombosis after plaque rupture. This is one of the possible reasons that cause thrombus,blood coagulation and disseminated intravascular coagulation (DIC) during septicemia.
