Hepatocyte Growth Factor Induces a Proangiogenic Phenotype and Mobilizes Endothelial Progenitor Cells by Activating Nox2

2011 ◽  
Vol 15 (4) ◽  
pp. 915-923 ◽  
Author(s):  
Katrin Schröder ◽  
Susanne Schütz ◽  
Isabella Schlöffel ◽  
Sina Bätz ◽  
Ina Takac ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor ◽  
Hepatocyte Growth

scholarly journals Up-regulation of Grb2-associated binder 1 promotes hepatocyte growth factor-induced endothelial progenitor cell proliferation and migration

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e6675
Author(s):  
Qing Fan ◽  
Liyu Zhang ◽  
Wenjie Zhu ◽  
Sheng Xue ◽  
Yisheng Song ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Adaptor Protein ◽  
Human Umbilical Cord ◽  
Endothelial Progenitor ◽  
And Migration ◽  
Hepatocyte Growth ◽  
Proliferation And Migration

Objectives Grb2-associated binder 1 (Gab1), a scaffolding adaptor protein, plays an important role in transmitting key signals that control cell growth, migration, and function from multiple tyrosine kinase receptors. This study was designed to investigate the influence of upregulation of Gab1 in endothelial progenitor cells (EPCs) stimulated with hepatocyte growth factor (HGF), and the underlying molecular mechanisms. Materials and Methods Endothelial progenitor cells isolated from human umbilical cord blood were identified and divided into four groups. EPCs in the Control group were cultured normally; those in the Control+HGF group were treated with HGF stimulation; those in the AD-Gab1 group were transfected with adenovirus containing the Gab1 gene but not treated with HGF stimulation; and, those in the AD-Gab1+HGF group were treated with both HGF stimulation and transfection with adenovirus containing the Gab1 gene. Subsequently, Gab1 expression and proliferation and migration ability were compared for EPCs grown under different conditions. Furthermore, we measured phosphorylation levels of three key proteins Gab1, SHP2, and ERK1/2. Results The AD-Gab1+HGF group had the highest expression of Gab1 and higher proliferation and migration than the other three groups. Conclusions Upregulation of Gab1 promoted HGF-induced EPC proliferation and migration. Mechanistically, HGF stimulated Gab1 tyrosine phosphorylation in EPCs, thus leading to activation of extracellular regulated MAP kinase 1/2, which is involved in proliferation and migration signaling.

Hepatocyte growth factor induces angiogenesis in injured lungs through mobilizing endothelial progenitor cells

2004 ◽  
Vol 324 (1) ◽  
pp. 276-280 ◽  
Author(s):  
Kota Ishizawa ◽  
Hiroshi Kubo ◽  
Mitsuhiro Yamada ◽  
Seiichi Kobayashi ◽  
Takashi Suzuki ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor ◽  
Hepatocyte Growth

Elevated Inflammatory Parameter Levels Negatively Impact Populations of Circulating Stem Cells (CD133+), Early Endothelial Progenitor Cells (CD133+/VEGFR2+), and Fibroblast Growth Factor in Stroke Patients

2019 ◽  
Vol 16 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Monika Golab-Janowska ◽  
Edyta Paczkowska ◽  
Boguslaw Machalinski ◽  
Dariusz Kotlega ◽  
Agnieszka Meller ◽  
...  
Keyword(s):  
Risk Factors ◽  
Stem Cells ◽  
Growth Factor ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Plasma Levels ◽  
Fibroblast Growth ◽  
Vascular Risk ◽  
Endothelial Progenitor ◽  
Inflammatory Parameters

Background: Endothelial Progenitor Cells (EPCs) are important players in neovascularization, mobilized through signalling by Angiogenic Growth Factors (AGFs) such as Vascular Endothelial Growth Factor (VEGF) and fibroblast growth factor (FGF). In vitro, inflammatory parameters impair the function and influence of EPCs on AGFs. However, this connection is not clear in vivo. To understand the mechanisms of augmented arteriogenesis and angiogenesis in acute ischemic stroke (AIS) patients, we investigated whether circulating stem cells (CD133+), early endothelial progenitor cells (CD133+/VEGFR2+), and endothelial cells (ECs; CD34¯/CD133¯/VEGFR2+) were increasingly mobilized during AIS, and whether there were correlations between EPC levels, growth factor levels and inflammatory parameters. Methods: Data on demographics, classical vascular risk factors, neurological deficit information (assessed using the National Institutes of Health Stroke Scale), and treatment were collected from 43 consecutive AIS patients (group I). Risk factor control patients (group II) included 22 nonstroke subjects matched by age, gender, and traditional vascular risk factors. EPCs were measured by flow cytometry and the populations of circulating stem cells (CD133+), early EPCs (CD133+/VEGFR2+), and ECs (CD34¯/CD133¯/VEGFR2+) were analysed. Correlations between EPC levels and VEGF and FGF vascular growth factor levels as well as the influence of inflammatory parameters on EPCs and AGFs were assessed. Results: Patient ages ranged from 54 to 92 years (mean age 75.2 ± 11.3 years). The number of circulating CD34¯/CD133¯/VEGF-R2+ cells was significantly higher in AIS patients than in control patients (p < 0.05). VEGF plasma levels were also significantly higher in AIS patients compared to control patients on day 7 (p < 0.05). FGF plasma levels in patients with AIS were significantly higher than those in the control group on day 3 (p < 0.05). There were no correlations between increased VEGF and FGF levels and the number of CD133+, CD133+/VEGFR2+, or CD34¯/CD133¯/VEGFR2+ cells. Leukocyte levels, FGF plasma levels, and the number of early EPCs were negatively correlated on day 3. High sensitivity C-reactive protein levels and the number of CD133+ and CD133+/VEGFR2+ cells were negatively correlated on day 7. In addition, there was a negative correlation between fibrinogen levels and FGF plasma levels as well as the number of early EPCs (CD133+/VEGFR2+). Conclusion: AIS patients exhibited increased numbers of early EPCs (CD133+/VEGFR2+) and AGF (VEGF and FGF) levels. A negative correlation between inflammatory parameters and AGFs and EPCs indicated the unfavourable influence of inflammatory factors on EPC differentiation and survival. Moreover, these correlations represented an important mechanism linking inflammation to vascular disease.

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