A Hybrid Model of the Role of VEGF Binding in Endothelial Cell Migration and Capillary Formation

Jain, Harsh; Jackson, Trachette L.

doi:10.3389/fonc.2013.00102

Cited by 16 publications

(13 citation statements)

References 87 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been reported that VEGF and IL-8 can promote endothelial cell migration in an autocrine manner [15, 16]. In our system, cell migration rate of HUVECs was accelerated after CM treatment compared with that of the control.…”

Section: Discussionsupporting

confidence: 54%

“…VEGF and IL-8 secreted by cancer cells act as chemoattractants in promoting motility of endothelial cell during tumor angiogenesis [12-14]. It is noteworthy that VEGF and IL-8 are secreted not only by tumor cells, but also by endothelial cells, thereby enhancing endothelial cell migration and angiogenesis [15, 16] . However, the molecular mechanisms underlying the effect of autocrine VEGF and IL-8 on endothelial cell migration are not completely understood to date.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Autocrine VEGF and IL-8 Promote Migration via Src/Vav2/Rac1/PAK1 Signaling in Human Umbilical Vein Endothelial Cells

Li¹,

Zhou²,

Jiang³

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Pro-angiogenic factors VEGF and IL-8 play a major role in modulating the migratory potential of endothelial cells. The goal of this study was to investigate the effect of autocrine VEGF and IL-8 in the form of self-conditioned medium (CM) on human umbilical vein endothelial cells (HUVECs). Methods: Enzyme-linked immunosorbent assay (ELISA) examined the automatic secretion of VEGF and IL-8 protein by HUVECs. Western blot, small interfering RNA (siRNA), pulldown and Transwell assays were used to explore the role and the mechanism of autocrine VEGF and IL-8 in migration of HUVECs. Results: Neutralizing VEGF and IL-8 in CM significantly abrogated CM-induced migration of HUVECs. Autocrine VEGF and IL-8 increased Src phosphorylation, Rac1 activity and PAK1 phosphorylation in a time dependent manner. Additionally, blocking Rac1 activity with Rac1 siRNA largely abolished autocrine VEGF and IL-8-induced cell migration. Vav2 siRNA suppressed autocrine VEGF and IL-8-induced Rac1 activation and cell migration. Furthermore, blocking Src signaling with PP2, a specific inhibitor for Src, markedly prevented autocrine VEGF and IL-8-induced Vav2 and Rac1 activation as well as consequently cell migration. PAK1 siRNA also significantly abolished autocrine VEGF and IL-8-induced cell migration. Conclusions: We demonstrated for the first time that autocrine VEGF and IL-8 promoted endothelial cell migration via the Src/Vav2/Rac1/PAK1 signaling pathway. This finding reveals the molecular mechanism in the increase of endothelial cell migration induced by autocrine growth factors and cytokines, which is expected to provide a novel therapeutic target in vascular diseases.

show abstract

Section: Discussionsupporting

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Autocrine VEGF and IL-8 Promote Migration via Src/Vav2/Rac1/PAK1 Signaling in Human Umbilical Vein Endothelial Cells

Li¹,

Zhou²,

Jiang³

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Moreover, hybrid models proposed to map VEGF-depended angiogenesis consider that VEGF concentration changes in addition to modeling che-motaxis of endothelial cells using the reinforced random walk. For example, it is reported that the hybrid model was able to predict the threshold concentration required to stimulate the quiet cells for a biased motion, as well as the optimum concentration for their movement [83].…”

Section: Reinforced Random Walkmentioning

confidence: 99%

Untitled

2018

Multidiscip Cancer Investig

View full text Add to dashboard Cite

Impairments in cell migration processes may cause various diseases, among which cancer cell metastasis, tumor angiogenesis, and the disability of immune cells to infiltrate into tumors are prominent ones. Mathematical modeling has been widely used to analyze the cell migration process. Cell migration is a complicated process and requires statistical methods such as random walk for proper analysis. In this study, we reviewed the studies conducted on the random walk-based stochastic modeling of the eukaryotic cell migration. This statistical modeling can open some perspectives on more detailed modeling approaches and ultimately lead to more comprehensive knowledge about the biophysical and biochemical foundations of cell migration process.

show abstract

“…Using all of these assays, enamel matrix derivative was found to possess pro‐angiogenesis properties . These assays were used to test other growth factors, such as vascular endothelial growth factor, epidermal growth factor, fibroblast growth factor and platelet‐derived growth factor . Alternatively, enamel matrix derivative could promote angiogenesis by inducing the expression of pro‐angiogenesis molecules, such as vascular endothelial growth factor, in different cells and this was demonstrated in gingival fibroblasts and periodontal ligament cells .…”

Section: In Vitro Models Of Soft‐tissue Wound Healingmentioning

confidence: 99%

In vitro models for evaluation of periodontal wound healing/regeneration

Weinreb¹,

Nemcovsky²

2015

Periodontology 2000

View full text Add to dashboard Cite

Periodontal wound healing and regeneration are highly complex processes, involving cells, matrices, molecules and genes that must be properly choreographed and orchestrated. As we attempt to understand and influence these clinical entities, we need experimental models to mimic the various aspects of human wound healing and regeneration. In vivo animal models that simulate clinical situations of humans can be costly and cumbersome. In vitro models have been devised to dissect wound healing/regeneration processes into discrete, analyzable steps. For soft tissue (e.g. gingival) healing, in vitro models range from simple culture of cells grown in monolayers and exposed to biological modulators or physical effectors and materials, to models in which cells are 'injured' by scraping and subsequently the 'wound' is filled with new or migrating cells, to three-dimensional models of epithelial-mesenchymal recombination or tissue explants. The cells employed are gingival keratinocytes, fibroblasts or endothelial cells, and their proliferation, migration, attachment, differentiation, survival, gene expression, matrix production or capillary formation are measured. Studies of periodontal regeneration also include periodontal ligament fibroblasts or progenitors, osteoblasts or osteoprogenitors, and cementoblasts. Regeneration models measure cellular proliferation, attachment and migration, as well as gene expression, transfer and differentiation into a mineralizing phenotype and biomineralization. Only by integrating data from models on all levels (i.e. a single cell to the whole organism) can various critical aspects of periodontal wound healing/regeneration be fully evaluated.

show abstract

A Hybrid Model of the Role of VEGF Binding in Endothelial Cell Migration and Capillary Formation

Cited by 16 publications

References 87 publications

Autocrine VEGF and IL-8 Promote Migration via Src/Vav2/Rac1/PAK1 Signaling in Human Umbilical Vein Endothelial Cells

Autocrine VEGF and IL-8 Promote Migration via Src/Vav2/Rac1/PAK1 Signaling in Human Umbilical Vein Endothelial Cells

Untitled

In vitro models for evaluation of periodontal wound healing/regeneration

Contact Info

Product

Resources

About