Hepatocyte Growth Factor Prevents Lipopolysaccharide-Induced Hepatic Sinusoidal Endothelial Cell Injury and Intrasinusoidal Fibrin Deposition in Rats

1998 ◽  
Vol 80 (2) ◽  
pp. 194-199 ◽  
Author(s):  
Shin-ichi Seto ◽  
Toshimi Kaido ◽  
Shoji Yamaoka ◽  
Akira Yoshikawa ◽  
Shigeki Arii ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cell Injury ◽  
Sinusoidal Endothelial Cell ◽  
Fibrin Deposition ◽  
Endothelial Cell Injury ◽  
Hepatic Sinusoidal Endothelial Cell ◽  
Hepatocyte Growth

Prognostic Significance of Plasma Hepatocyte Growth Factor in Sepsis

2021 ◽  
pp. 088506662199342
Author(s):  
Fei Peng ◽  
Chenglong Liang ◽  
Wei Chang ◽  
Qin Sun ◽  
Jianfeng Xie ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cell Injury ◽  
Prognostic Significance ◽  
Trial Registration ◽  
Enzyme Linked Immunosorbent Assay ◽  
Pulmonary Vascular Permeability ◽  
Endothelial Cell Injury ◽  
Hepatocyte Growth

Background: To assess any correlation of plasma hepatocyte growth factor (HGF) levels with relevant endothelial cell injury parameters and determine the prognostic value in septic patients. Methods: A prospective, observational study was conducted in patients with sepsis admitted to the Department of Critical Care Medicine at the Zhongda Hospital from November 2017 to March 2018. Plasma HGF levels were measured by enzyme-linked immunosorbent assay in the first 24 h after admission (day 1) and on day 3. The primary endpoint was defined as all-cause 28-day mortality. Furthermore, we analyzed the correlation of HGF with relevant endothelial cell injury markers. Results: Eighty-six patients admitted with sepsis were included. HGF levels of nonsurvivors were elevated compared to those of survivors on day 1 (1940.62 ± 74.66 pg/mL vs. 1635.61 ± 47.49 pg/mL; P = 0.002) and day 3 (1824.82 ± 137.52 pg/mL vs. 1309.77 ± 83.49 pg/mL; P = 0.001) and showed a strong correlation with von Willebrand factor (r = 0.45, P < 0.0001), lactate (r = 0.35, P = 0.0011), pulmonary vascular permeability index (r = 0.38, P = 0.0241), first 24 h fluid administration (r = 0.38, P < 0.0001), and sequential organ failure assessment score (r = 0.40, P = 0.0001). Plasma HGF levels were able to prognostically discriminate between survivors and nonsurvivors on day 1 (AUC: 0.72, 95%CI: 0.60-0.84) and day 3 (AUC: 0.77, 95%CI: 0.63-0.91). Conclusions: HGF levels are associated with sepsis and correlated with established markers of endothelial cell injury. Elevated HGF levels in sepsis patients are an efficient indicator of poor prognosis. Trial registration: The study was registered in Clinical Trial (Registration Number: NCT02883231).

Sinusoidal endothelial cell injury by superoxide anion and iron in the Propionibacterium acnes -pretreated and lipopolysaccharide-stimulated rat liver

2001 ◽  
Vol 21 (6) ◽  
pp. 415-424 ◽  
Author(s):  
Tadashi Hasegawa ◽  
Minoru Nakano ◽  
Takashi Hashimoto ◽  
Katsuya Hiraishi ◽  
Keiji Suzuki ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Rat Liver ◽  
Superoxide Anion ◽  
Cell Injury ◽  
Propionibacterium Acnes ◽  
Sinusoidal Endothelial Cell ◽  
Endothelial Cell Injury

scholarly journals Monocyte activation state regulates monocyte-induced endothelial proliferation through Met signaling

Blood ◽  
2010 ◽  
Vol 115 (16) ◽  
pp. 3407-3412 ◽  
Author(s):  
Shai Y. Schubert ◽  
Alejandro Benarroch ◽  
Juan Monter-Solans ◽  
Elazer R. Edelman
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Direct Interaction ◽  
Endothelial Cell Proliferation ◽  
Specific Cell ◽  
Mrna Levels ◽  
Hepatocyte Growth

Abstract Direct interaction of unactivated primary monocytes with endothelial cells induces a mitogenic effect in subconfluent, injured endothelial monolayers through activation of endothelial Met. We now report that monocytes' contact-dependent mitogenicity is controlled by activation-mediated regulation of hepatocyte growth factor. Direct interaction of unactivated monocytes with subconfluent endothelial cells for 12 hours resulted in 9- and 120-fold increase in monocyte tumor necrosis factor-α (TNFα) and interleukin-1β (IL-1β) mRNA levels and bitemporal spike in hepatocyte growth factor that closely correlates with endothelial Met and extracellular signal-related kinase (ERK) phosphorylation. Once activated, monocytes cannot induce a second wave of endothelial cell proliferation and endothelial Met phosphorylation and soluble hepatocyte growth factor levels fall off. Monocyte-induced proliferation is dose dependent and limited to the induction of a single cell cycle. Monocytes retain their ability to activate other endothelial cells for up to 8 hours after initial interaction, after which they are committed to the specific cell. There is therefore a profoundly sophisticated mode of vascular repair. Confluent endothelial cells ensure vascular quiescence, whereas subconfluence promotes vessel activation. Simultaneously, circulating monocytes stimulate endothelial cell proliferation, but lose this potential once activated. Such a system provides for the fine balance that can restore vascular and endothelial homeostasis with minimal overcompensation.

scholarly journals Liver sinusoidal endothelial cell injury by neutrophils in rats with acute obstructive cholangitis

2002 ◽  
Vol 8 (2) ◽  
pp. 342 ◽  
Author(s):  
Jian-Ping Gong ◽  
Chuan-Xin Wu ◽  
Chang-An Liu ◽  
Sheng-Wei Li ◽  
Yu-Jun Shi ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Injury ◽  
Sinusoidal Endothelial Cell ◽  
Liver Sinusoidal Endothelial Cell ◽  
Endothelial Cell Injury ◽  
Obstructive Cholangitis
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