W03-P-007 Hepatocyte growth factor-induced signaling in endothelial cell proliferation

2005 ◽  
Vol 6 (1) ◽  
pp. 14
Author(s):  
C.R.W. Kuhlmann ◽  
A. Fehsecke ◽  
C.A. Schaefer ◽  
A.K. Most ◽  
H. Tillmanns ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Endothelial Cell Proliferation ◽  
Hepatocyte Growth

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 Hepatocyte Growth Factor Overexpression in the Islet of Transgenic Mice Increases Beta Cell Proliferation, Enhances Islet Mass, and Induces Mild Hypoglycemia

2000 ◽  
Vol 275 (2) ◽  
pp. 1226-1232 ◽  
Author(s):  
Adolfo Garcia-Ocaña ◽  
Karen K. Takane ◽  
Mushtaq A. Syed ◽  
William M. Philbrick ◽  
Rupangi C. Vasavada ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Transgenic Mice ◽  
Hepatocyte Growth Factor ◽  
Beta Cell ◽  
Beta Cell Proliferation ◽  
Islet Mass ◽  
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).

scholarly journals Comparative Effects of Basic Fibroblast Growth Factor Delivery or Voluntary Exercise on Muscle Regeneration after Volumetric Muscle Loss

2022 ◽  
Vol 9 (1) ◽  
pp. 37
Author(s):  
Caroline Hu ◽  
Bugra Ayan ◽  
Gladys Chiang ◽  
Alex H. P. Chan ◽  
Thomas A. Rando ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Muscle Regeneration ◽  
Collagen Scaffold ◽  
Voluntary Exercise ◽  
Endothelial Cell Proliferation ◽  
Fibroblast Growth ◽  
Muscle Loss ◽  
Volumetric Muscle Loss

Volumetric muscle loss (VML) is associated with irreversibly impaired muscle function due to traumatic injury. Experimental approaches to treat VML include the delivery of basic fibroblast growth factor (bFGF) or rehabilitative exercise. The objective of this study was to compare the effects of spatially nanopatterned collagen scaffold implants with either bFGF delivery or in conjunction with voluntary exercise. Aligned nanofibrillar collagen scaffold bundles were adsorbed with bFGF, and the bioactivity of bFGF-laden scaffolds was examined by skeletal myoblast or endothelial cell proliferation. The therapeutic efficacy of scaffold implants with either bFGF release or exercise was examined in a murine VML model. Our results show an initial burst release of bFGF from the scaffolds, followed by a slower release over 21 days. The released bFGF induced myoblast and endothelial cell proliferation in vitro. After 3 weeks of implantation in a mouse VML model, twitch force generation was significantly higher in mice treated with bFGF-laden scaffolds compared to bFGF-laden scaffolds with exercise. However, myofiber density was not significantly improved with bFGF scaffolds or voluntary exercise. In contrast, the scaffold implant with exercise induced more re-innervation than all other groups. These results highlight the differential effects of bFGF and exercise on muscle regeneration.

scholarly journals Endostatin: A Promising Drug for Antiangiogenic Therapy

1999 ◽  
Vol 14 (4) ◽  
pp. 263-267 ◽  
Author(s):  
L. Cirri ◽  
S. Donnini ◽  
L. Morbidelli ◽  
P. Chiarugi ◽  
M. Ziche ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Antiangiogenic Therapy ◽  
Specific Inhibitor ◽  
Angiogenesis Inhibitors ◽  
Endothelial Cell Proliferation ◽  
Platelet Factor ◽  
Collagen Xviii ◽  
And Migration

Angiogenesis, the formation of new blood vessels from existing capillaries, is critical for tumors to grow beyond a few in size. Tumor cells produce one or more angiogenic factors including fibroblast growth factor and vascular endothelial growth factor. Surprisingly, antiangiogenic factors or angiogenesis inhibitors have been isolated from tumors. Some angiogenesis inhibitors, such as angiostatin, are associated with tumors while others, such as platelet-factor 4 and interferon-alpha are not. Endostatin, a C-terminal product of collagen XVIII, is a specific inhibitor of endothelial cell proliferation, migration and angiogenesis. The mechanism by which endostatin inhibits endothelial cell proliferation and migration is unknown. Endostatin was originally expressed in a prokaryotic system and, late, in a yeast system, thanks to which it is possible to obtain a sufficient quantity of the protein in a soluble and refolded form to be used in preclincial and clinical trials.

Hepatocyte growth factor plays a dual role in tendon‐derived stem cell proliferation, migration, and differentiation

2019 ◽  
Vol 234 (10) ◽  
pp. 17382-17391 ◽  
Author(s):  
Peilin Han ◽  
Qingbo Cui ◽  
Wenjun Lu ◽  
Shulong Yang ◽  
Manyu Shi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Dual Role ◽  
Stem Cell Proliferation ◽  
Hepatocyte Growth
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